l'amiante chrysotile

ISBN 978-92-4-256481-5

L’amiante – un groupe de minéraux comportant le chrysotile, la

crocidolite, l’amosite, l’anthophyllite, la trémolite et l’actinolite – est

l’un des produits cancérogènes les plus importants sur les lieux de

travail. Au moins 107 000 personnes meurent chaque année de

maladies liées à l’amiante, dont le cancer du poumon. Même

si son utilisation a beaucoup baissé dans de nombreux pays, le

chrysotile reste largement employé, en particulier dans les pays

en développement.

La présente publication sur l’amiante chrysotile comporte trois par-

ties. La première reproduit un bref document d’information de

l’OMS à l’intention des décideurs sur l’élimination des maladies liées

à l’amiante. La deuxième répond aux questions soulevées

couramment au cours des discussions politiques, en particulier pour

aider les décideurs. La troisième est un résumé technique des effets

du chrysotile sur la santé, réunissant et récapitulant pour la première

fois les évaluations les plus récentes de l’OMS qui font autorité et

ont été réalisées par son Centre international de recherche sur le

cancer et son Programme international sur la sécurité chimique. Ce

résumé technique passe également en revue les résultats des prin-

cipales études publiées après ces évaluations, ainsi que les con-

clusions tirées des évaluations des produits de remplacement

faites par l’OMS.

Cette publication intéressera tous les responsables gouvernementaux

devant prendre des décisions éclairées sur la gestion des risques san-

itaires liés à l’exposition à l’amiante chrysotile.

Département Santé publique, environnement et déterminants sociaux de la santé (PHE)

Santé de la famille, de la femme et de l’enfant (FWC)

Organisation mondiale de la Santé (OMS)

Avenue Appia 20 – CH-1211 Genève 27 – Suisse

www.who.int/phe/fr/

www.who.int/ipcs/fr/

Courriel : [email protected]

L’amiante chrysotileSANTÉ PUBLIQUE ET ENVIRONNEMENT

Pour obtenir plus d’informations de l’OMS sur les produits chimiques ayant une

importance majeure en santé publique, parmi lesquels l’amiante, consulter le

site suivant :

http://www.who.int/ipcs/assessment/public_health/chemicals_phc

L’amiante chrysotile

Catalogage à la source : Bibliothèque de l’OMS

L’amiante chrysotile.

1. Amiante serpentine. 2. Exposition environnementale. 3. Exposition professionnelle.

4. Tumeurs – prévention et contrôle. I.Organisation mondiale de la Santé.

ISBN 978 92 4 256481 5 (Classification NLM : WA 754)

© Organisation mondiale de la Santé 2014

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Les appellations employées dans la présente publication et la présentation des données qui y figurent n’im-

pliquent de la part de l’Organisation mondiale de la Santé aucune prise de position quant au statut juridique des

pays, territoires, villes ou zones, ou de leurs autorités, ni quant au tracé de leurs frontières ou limites. Les traits

discontinus formés d’une succession de points ou de tirets sur les cartes représentent des frontières approxi-

matives dont le tracé peut ne pas avoir fait l’objet d’un accord définitif.

La mention de firmes et de produits commerciaux ne signifie pas que ces firmes et ces produits commerciaux

sont agréés ou recommandés par l’Organisation mondiale de la Santé, de préférence à d’autres de nature ana-

logue. Sauf erreur ou omission, une majuscule initiale indique qu’il s’agit d’un nom déposé.

L’Organisation mondiale de la Santé a pris toutes les précautions raisonnables pour vérifier les informations

contenues dans la présente publication. Toutefois, le matériel publié est diffusé sans aucune garantie, expresse

ou implicite. La responsabilité de l’interprétation et de l’utilisation dudit matériel incombe au lecteur. En aucun

cas, l’Organisation mondiale de la Santé ne saurait être tenue responsable des préjudices subis du fait de son

utilisation.

La production, la traduction et la publication du présent document ont reçu l’appui financier du programme

de Fonds de développement international de la Mission permanente de l’Australie auprès des Nations Unies,

du Gouvernement allemand et de la Commission européenne. Les opinions exprimées dans la publication ne

représentent pas nécessairement celles de ces organisations.

Crédits photos :

Couverture, pages iv, 8, 10, 14, 15, 17, 19, 20, 23, 29, 30, 32, 34, 35, 36, 37 © OMS / R. Moore;

page 1 © Microlabgallery.com; page 3 © I. Masayuki; pages 4, 33 © P. Madhavan;

page 6 © U.S. Geological Survey / A. Silver; pages 9, 11, 25 © M. Darisman; pages 24, 27 © S. Furuya;

page 34 (fibres) © U.S. Geological Survey

Graphisme : Inís Communication – www.iniscommunication.com

L’AMIANTE CHRYSOTILE / iii

Table des matièresAvant-propos ...................................................................................... 1

Élimination des maladies liées à l’amiante .............................................. 2

Questions fréquemment posées et réponses ............................................. 6

Informations complémentaires ............................................................. 12

Technical summary of WHO evaluations of chrysotile .............................. 13

iv / L’AMIANTE CHRYSOTILE

L’AMIANTE CHRYSOTILE / 1

Avant-proposBeaucoup de pays ont déjà pris des mesures au niveau national pour

interdire l’usage de l’amiante sous toutes ses formes, afin de limiter

l’exposition et de combattre, éviter et, au bout du compte, éliminer les

maladies liées à l’amiante, à l’origine d’au moins 107 000 décès par an

dans le monde. Il reste cependant un certain nombre de pays qui, pour

diverses raisons, n’ont pas encore agi en ce sens. En gardant cela à l’es-

prit, la présente publication a pour première raison d’être d’aider les États

Membres de l’Organisation mondiale de la Santé (OMS) à prendre des déci-

sions éclairées sur la gestion des risques sanitaires liés à l’exposition à l’amiante

chrysotile.

Le document se divise en trois parties. La première reproduit un bref document d’information

de l’OMS à l’intention des décideurs sur l’élimination des maladies liées à l’amiante, actua-

lisé en mars 2014. La deuxième répond aux questions soulevées couramment au cours des

discussions politiques, avec le but spécifique d’aider les décideurs à se forger une opinion.

La troisième est un résumé technique des effets du chrysotile sur la santé, qui rassemble et

récapitule pour la première fois les évaluations les plus récentes de l’OMS qui font autorité et

ont été réalisées par son Centre international de Recherche sur le Cancer et son Programme

international sur la sécurité chimique. Le résumé technique passe également en revue les

résultats des principales études publiées après ces évaluations puis, brièvement, les conclu-

sions tirées des évaluations des produits de remplacement faites par l’OMS.

Je recommande la lecture de cette publication aux ministres, responsables gouvernementaux

et aux autres personnes souhaitant ou devant prendre des décisions sur l’amiante et en par-

ticulier le chrysotile, ainsi que sur les conséquences de l’exposition pour la santé, ou rendre

un avis à ce sujet.

Dr Maria NeiraDirecteur, Département Santé publique, environnement et déterminants sociaux de la santé

Organisation mondiale de la Santé, Genève

2 / L’AMIANTE CHRYSOTILE

Élimination des maladies liées à l’amianteMise à jour de mars 2014

L’amiante est l’un des produits cancérogènes les plus importants sur les lieux de travail,

puisqu’il est responsable de près de la moitié des décès par cancer dus à une exposition pro-

fessionnelle (1, 2). En 2003, la treizième session du Comité mixte Organisation internationale

du Travail (OIT)/Organisation mondiale de la Santé (OMS) de la Médecine du travail a recom-

mandé d’accorder une attention particulière à l’élimination des maladies liées à l’amiante (3). En 2005, dans sa résolution WHA58.22 sur la lutte contre le cancer, l’Assemblée mondiale de

la Santé (AMS) a prié instamment les États Membres d’accorder une attention particulière aux

cancers pour lesquels le fait d’éviter l’exposition est un facteur important, notamment s’agis-

sant de l’exposition professionnelle et environnementale à des produits chimiques. En 2007,

l’AMS a demandé dans sa résolution WHA60.26 l’organisation de campagnes mondiales pour

éliminer les maladies liées à l’amiante et, en 2013, la résolution WHA66.10 traitait de la pré-

vention et de la maîtrise des maladies non transmissibles, dont le cancer.

Le terme « amiante » désigne un groupe de minéraux fibreux naturels (serpentine ou amphi-

bole) actuellement utilisés, ou l’ayant été dans le passé, dans le commerce à cause de leur

extraordinaire résistance à la traction, de leur mauvaise conduction de la chaleur et de leur

résistance relative aux attaques chimiques. Les principales variétés d’amiante sont le chryso-

tile, tiré de la serpentine, et la crocidolite, l’anthophyllite, la trémolite et l’actinolite, qui sont

des amphiboles (4).

L’exposition à l’amiante, chrysotile compris, provoque des cancers du poumon, du larynx, des

ovaires, le mésothéliome (un cancer des cellules tapissant la plèvre et le péritoine) et l’asbes-

tose (fibrose pulmonaire) (5–7).

L’exposition à l’amiante et ses répercussions en santé publique sont importantesIl y a exposition à l’amiante par inhalation de fibres présentes principalement dans l’air conta-

miné de l’environnement professionnel, ainsi que dans l’air ambiant à proximité de sources

ponctuelles d’amiante ou dans l’air à l’intérieur des habitations ou des bâtiments contenant

des matériaux amiantés friables. Les degrés d’exposition les plus élevés s’observent au cours

du reconditionnement des conteneurs d’amiante, du mélange avec d’autres produits bruts

ou de la coupe à sec, avec des outils abrasifs, de produits contenant de l’amiante. Il peut

également y avoir une exposition lors de l’installation et de l’utilisation de produits contenant

de l’amiante et de l’entretien des véhicules. Il y a toujours dans de nombreux bâtiments des

matériaux friables contenant du chrysolite et/ou de l’amphibole qui continuent de donner lieu

à des expositions à ces substances lors des opérations d’entretien, de réparation, de dépose

et de démolition (5). Des expositions peuvent aussi survenir à la suite de catastrophes natu-

relles endommageant les bâtiments.

L’amiante est l’un des produits cancérogènes les plus importants sur les lieux de travail


Actuellement, près de 125 millions de personnes dans le monde sont exposées à l’amiante

sur le lieu de leur travail (1). D’après les estimations mondiales, 107 000 personnes au

moins meurent chaque année de cancer du poumon, de mésothéliome ou d’asbestose liés à

l’amiante dans le cadre d’expositions professionnelles (1, 2, 8). De plus, près de 400 décès

ont été attribués à des expositions non professionnelles à l’amiante. Le poids des maladies

liées à l’amiante continue de s’alourdir, même dans les pays qui en ont interdit l’utilisation au

début des années 1990. Du fait des longues périodes de latence des maladies en question,

l’arrêt de l’utilisation de l’amiante aujourd’hui n’entraînera une baisse du nombre des décès

liés à l’amiante qu’au bout d’un certain nombre de décennies.

Tous les types d’amiante sont cancérogènes pour l’hommeLe Centre international de Recherche sur le Cancer a classé l’amiante (actinolite, amosite,

anthophyllite, chrysotile, crocidolite et trémolite) dans les produits cancérogènes pour l’homme

(7). L’exposition au chrysotile, à l’amosite et à l’anthophyllite, ainsi qu’à des mélanges renfer-

mant de la crocidolite, entraîne un risque accru de cancer du poumon (7). On a observé des

mésothéliomes après des expositions professionnelles à la crocidolite, à l’amosite, à la trémo-

lite et au chrysotile, ainsi que dans la population générale vivant dans le voisinage d’usines et

de mines d’amiante et dans l’entourage des ouvriers travaillant l’amiante (7).

L’incidence des maladies liées à l’amiante est fonction du type, de la taille et de la dose de

fibres, ainsi que du traitement industriel de l’amiante (6). Aucun seuil n’a été mis en évidence

pour le risque cancérogène de l’amiante, chrysotile compris (5, 7). Le tabagisme augmente le

risque de cancer pulmonaire résultant de l’exposition à l’amiante (5, 9).

Le chrysotile est toujours largement utiliséOn a utilisé l’amiante dans des milliers de produits pour un très grand nombre d’applications :

bardeaux de toiture, canalisations d’eau, couvertures antifeu et matériaux isolants, garnitures

de disques d’embrayage et de freins, joints d’étanchéité et plaquettes pour les automobiles.

À la suite des inquiétudes croissantes quant aux effets sur la santé, l’utilisation de l’amiante

a reculé dans de nombreux pays. L’emploi de la crocidolite et des produits contenant cette

fibre, ainsi que la pulvérisation de toutes les formes d’amiante ont été interdits à partir de

1986 dans le cadre de la Convention N° 162 de l’OIT relative à la sécurité de l’utilisation de

l’amiante. Mais le chrysotile reste toujours largement employé, près de 90 % l’étant dans les

matériaux de construction à base d’amiante-ciment, dont les pays en développement sont les

plus grands utilisateurs. Il subsiste d’autres usages du chrysotile : matériaux de friction (7 %),

textiles et autres applications (10).

À ce jour (fin 2013), plus de 50 pays, dont tous les États Membres de l’Union Européenne,

ont interdit l’utilisation de l’amiante sous toutes ses formes, chrysotile compris. D’autres pays

ont introduit des limitations moins strictes, tandis que certains ont maintenu, voire augmenté,

leur production ou leur utilisation de chrysotile ces dernières années (11). C’est dans la

Région Asie-Pacifique que l’usage a le plus augmenté. La production mondiale d’amiante

sur la période 2000–2012 est restée relativement stable, à environ 2 millions de tonnes par

an (12, 13).

107 000 personnes au moins meurent chaque année de cancer du poumon, de mésothéliome ou d’asbestose liés à l’amiante dans le cadre d’expositions professionnelles


Recommandations de l’OMS relatives à la prévention des maladies liées à l’amianteSachant que l’on n’a aucune preuve de l’existence d’un seuil pour l’effet cancérogène de

l’amiante, chrysotile compris, et que l’on a observé une augmentation du risque de cancer

dans les populations très faiblement exposées (5, 7), la façon la plus efficace d’éliminer les

maladies liées à l’amiante consiste à mettre fin à l’emploi de ce produit sous toutes ses formes.

La poursuite de l’utilisation de l’amiante-ciment dans le secteur de la construction est parti-

culièrement préoccupante du fait de la main d’œuvre importante, de la difficulté de contrôler

l’exposition et de la possibilité de dégradation des matériaux en place, ce qui constitue un

risque pour ceux qui apportent des modifications ou procèdent à des opérations d’entretien

ou de démolition (5). L’amiante peut être remplacé dans ses diverses applications par des

matières fibreuses (14) et d’autres produits avec moins ou pas de risque pour la santé.

Les matériaux contenant de l’amiante doivent être encapsulés et,

en général, il n’est pas recommandé de procéder à des travaux

risquant de toucher les fibres. S’ils sont nécessaires, ils ne seront

effectués que dans le cadre de strictes mesures de contrôle pour

éviter toute exposition : par exemple l’encapsulation, les procédés

humides, une ventilation aspirante locale avec filtration et le net-

toyage régulier. Ils exigent également le port d’un équipement de

protection individuelle : appareils respiratoires spéciaux, lunettes

de protection, gants et vêtements protecteurs, ainsi que la mise

en place d’installations spéciales pour la décontamination (15).

L’OMS s’est engagée à collaborer avec les pays pour éliminer les

maladies liées à l’amiante dans le cadre des orientations straté-

giques suivantes :

• reconnaître que la façon la plus efficace d’éliminer ces maladies consiste à mettre fin à

l’utilisation de l’amiante sous toutes ses formes ;• fournir des informations sur les solutions permettant de remplacer l’amiante par des pro-

duits plus sûrs et développer des mécanismes économiques et technologiques favorisant

cette substitution ;• prendre des mesures pour éviter toute exposition à l’amiante en place et au cours des opé-

rations d’élimination (réduction) ;• améliorer les services de diagnostic précoce, de traitement et de réadaptation pour les

maladies liées à l’amiante et établir des registres des personnes ayant été exposées à

l’amiante et/ou l’étant encore.

L’OMS recommande fortement la planification et la mise en œuvre de ces mesures dans le

cadre d’une approche nationale exhaustive visant à éliminer les maladies liées à l’amiante.

Une telle approche doit également comprendre l’élaboration de profils nationaux, la sensibi-

lisation, le renforcement des capacités, un cadre institutionnel et un plan d’action national

pour l’élimination des maladies liées à l’amiante.

L’OMS collaborera avec l’OIT à la mise en œuvre de la résolution sur l’amiante, adoptée à

la quatre-vingt-quinzième session de la Conférence internationale du Travail (16) et avec

d’autres organisations intergouvernementales et la société civile en vue d’éliminer les mala-

dies liées à l’amiante dans le monde entier.


Références1. Concha-Barrientos M, Nelson D, Driscoll T, Steenland N, Punnett L, Fingerhut M et al. Chapter 21. Selected

occupational risk factors. In: Ezzati M, Lopez A, Rodgers A, Murray C, editors. Comparative quantification of health risks: global and regional burden of disease attributable to selected major risk factors. Genève : Organisation mondiale de la Santé ; 2004:1651–801 (http://www.who.int/healthinfo/global_burden_disease/cra/en/, consulté le 11 mars 2014).

2. Driscoll T, Nelson DI, Steenland K, Leigh J, Concha-Barrientos M, Fingerhut M et al. The global burden of disease due to occupational carcinogens. Am J Ind Med. 2005;48(6):419–31.

3. OIT, OMS. Rapport de la treizième session du Comité mixte OIT/OMS de la Médecine du Travail, 9–12 décembre 2003, Genève. JCOH/2003/D.4. Genève : Bureau international du Travail ; 2003 (http://www.ilo.org/wcmsp5/groups/public/---ed_protect/---protrav/---safework/documents/publication/wcms_110478.pdf, consulté le 13 mars 2014).

4. 6.2 Asbestos. In: Air quality guidelines for Europe, second edition. Publications régionales de l’OMS, Série européenne, No. 91. Copenhague : Bureau régional OMS de l’Europe ; 2000 (http://www.euro.who.int/__data/assets/pdf_file/0005/74732/E71922.pdf, consulté le 11 mars 2014).

5. Environmental Health Criteria 203: Chrysotile asbestos. Genève : Organisation mondiale de la Santé, Programme international sur la sécurité chimique; 1998 (http://www.inchem.org/documents/ehc/ehc/ehc203.htm, consulté le 11 mars 2014).

6. Environmental Health Criteria 53: Asbestos and other natural mineral fibres. Genève : Organisation mondiale de la Santé, Programme international sur la sécurité chimique ; 1986 (http://www.inchem.org/documents/ehc/ehc/ehc53.htm, consulté le 13 mars 2014).

7. Centre international de Recherche sur le Cancer. Asbestos (chrysotile, amosite, crocidolite, trémolite, actinolite, and anthophyllite). IARC Monogr Eval Carcinog Risks Hum. 2012;100C:219–309 (http://monographs.iarc.fr/ENG/Monographs/vol100C/index.php, consulté le 11 mars 2014).

8. Driscoll T, Nelson DI, Steenland K, Leigh J, Concha-Barrientos M, Fingerhut M et al. The global burden of non-malignant respiratory disease due to occupational airborne exposures. Am J Ind Med. 2005;48(6):432–45.

9. Centre international de Recherche sur le Cancer. Tobacco smoke and involuntary smoking. IARC Monogr Eval Carcinog Risks Hum. 2006;83.

10. Perron L. Chrysotile. In: Canadian minerals yearbook, 2003. Ottawa: Natural Resources Canada; 2003:18.1–18.11.

11. Virta RL. Worldwide asbestos supply and consumption trends from 1900 through 2003. Circular 1298. Reston (VA): United States Department of the Interior, United States Geological Survey; 2006 (http://pubs.usgs.gov/circ/2006/1298/c1298.pdf, consulté le 11 mars 2014).

12. Virta RL. Asbestos [Advance release]. In: 2012 minerals yearbook. Reston (VA): United States Department of the Interior, United States Geological Survey; 2013:8.1–8.7 (http://minerals.usgs.gov/minerals/pubs/commodity/asbestos/myb1-2012-asbes.pdf, consulté le 11 mars 2014).

13. Virta RL. Asbestos statistics and information. In: Mineral commodity summaries 2013. Reston (VA): United States Department of the Interior, United States Geological Survey; 2013 (http://minerals.usgs.gov/minerals/pubs/commodity/asbestos/mcs-2013-asbes.pdf, consulté le 11 mars 2014).

14. Summary consensus report of WHO Workshop on Mechanisms of Fibre Carcinogenesis and Assessment of Chrysotile Asbestos Substitutes, 8–12 November 2005, Lyon. Genève: Organisation mondiale de la Santé ; 2005 (http://www.who.int/ipcs/publications/new_issues/summary_report.pdf, consulté le 11 mars 2014).

15. International Chemical Safety Card 0014: Chrysotile. Genève: Organisation mondiale de la Santé, Programme international sur la sécurité chimique ; 2010 (http://www.inchem.org/documents/icsc/icsc/eics0014.htm, consulté le 13 mars 2014).

16. Annexe : Résolution concernant l’amiante. Dans : Compte rendu provisoire 20 de la quatre-vingt-quinzième session, Conférence internationale du Travail, 31 mai – 16 juin 2006, Genève : Rapport de la Commission de la sécurité et de la santé. Genève : Organisation internationale du Travail ; 2006:20/69 (http://www.ilo.org/public/french/standards/relm/ilc/ilc95/pdf/pr-20.pdf, consulté le 13 mars 2014).

http://www.ilo.org/wcmsp5/groups/public/---ed_protect/---protrav/---safework/documents/publication/wcms_110478.pdf

http://www.ilo.org/wcmsp5/groups/public/---ed_protect/---protrav/---safework/documents/publication/wcms_110478.pdf

http://pubs.usgs.gov/circ/2006/1298/c1298.pdf


http://pubs.usgs.gov/circ/2006/1298/c1298.pdf%2C%20consult%C3%A9%20le%2011%20mars%202014

http://minerals.usgs.gov/minerals/pubs/commodity/asbestos/myb1-2012-asbes.pdf


http://minerals.usgs.gov/minerals/pubs/commodity/asbestos/myb1-2012-asbes.pdf%2C%20consult%C3%A9%20le%2011%20mars%202014

http://minerals.usgs.gov/minerals/pubs/commodity/asbestos/mcs-2013-asbes.pdf


http://minerals.usgs.gov/minerals/pubs/commodity/asbestos/mcs-2013-asbes.pdf%2C%20consult%C3%A9%20le%2011%20mars%202014


Questions fréquemment posées et réponsesNous allons répondre dans cette section aux questions fréquemment posées par les décideurs politiques à propos de l’utilisation du chrysotile.

Est-il vrai que le chrysotile n’est pas réellement une forme d’amiante ?

Non, c’est l’une des six formes d’amiante, les autres étant la crocidolite, l’amosite, la trémo-

lite, l’actinolite et l’anthophyllite.

Quelle est la politique de l’OMS en matière d’amiante ?

La politique de l’OMS à ce sujet est sans équivoque. L’amiante provoque des cancers du pou-

mon, du larynx, de l’ovaire, le mésothéliome (un cancer des cellules tapissant la plèvre et le

péritoine) et l’asbestose (fibrose pulmonaire). On peut et doit prévenir les maladies liées à

l’amiante et le moyen le plus efficace pour y arriver est de mettre fin à l’utilisation de toutes

les formes d’amiante pour éviter l’exposition. Les campagnes mondiales de l’OMS pour élimi-

ner les maladies liées à l’amiante visent à aider les pays à atteindre cet objectif.

Pourquoi l’OMS se préoccupe-t-elle autant de l’amiante ?

On a des preuves scientifiques indubitables que l’amiante provoque des cancers et des mala-

dies respiratoires chroniques chez l’homme. L’OMS travaille pour réduire le fardeau mondial

des maladies non transmissibles, parmi lesquelles le cancer et les maladies respiratoires

chroniques, reconnaissant que la prévention primaire réduit les coûts pour les services de

santé et aide à garantir que les dépenses de santé se maintiennent à un niveau viable. À

l’échelle mondiale, le cancer est la deuxième cause de mortalité. En 2008, il y a eu 7,6 mil-

lions de décès par cancer et 12,7 millions de nouveaux cas. En gros, on estime qu’on peut

attribuer 19 % des cancers à des causes liés à l’environnement, dont le milieu professionnel.

Actuellement, environ 125 millions de personnes dans le monde sont exposées à l’amiante sur

leur lieu de travail. D’après les estimations de l’OMS, au moins 107 000 personnes meurent

chaque année de cancer pulmonaire, de mésothéliome ou d’asbestose liés à des expositions

professionnelles. On estime que l’amiante est à l’origine de la moitié des décès dus à des can-

cers imputables à une exposition professionnelle.

Quelle autorité l’OMS a-t-elle pour parler du chrysotile, des autres formes d’amiante et de la gestion de ces produits ?

Au sein du système des Nations Unies, l’OMS est l’autorité directrice et coordonnatrice dans

le domaine de la santé. Elle est chargée de diriger l’action sanitaire mondiale, de définir les

programmes de recherche en santé, de fixer des normes et des critères, de présenter des

options politiques fondées sur des données probantes, de fournir un soutien technique aux

pays et de suivre et d’apprécier les tendances en matière de santé publique.

Chrysotile à l’état brut


L’Assemblée mondiale de la Santé (AMS) est l’organe décisionnel suprême de l’OMS ; elle se

réunit chaque année et se compose des délégations des 194 États Membres. Sa principale

fonction consiste à arrêter la politique de l’Organisation.

La politique de l’OMS en matière d’amiante a été établie par trois résolutions de l’AMS :

WHA58.22 en 2005, WHA60.26 en 2007 et WHA66.10 en 2013. La résolution WHA58.22

porte sur les cancers dont l’étiologie est liée à une exposition évitable aux agents cancéro-

gènes, la résolution WHA60.26 demande une campagne mondiale pour l’élimination des

maladies liées à l’amiante et la résolution WHA66.10 traite de la prévention et de la maîtrise

des maladies non transmissibles, parmi lesquelles le cancer.

Comment s’expose-t-on à l’amiante ?

L’exposition à l’amiante survient par inhalation et, dans une moindre mesure, par ingestion

lors de l’extraction minière et du broyage du minerai, ainsi que lors de la production et de

l’utilisation des produits contenant de l’amiante. Cela inclut la découpe et la mise en place de

l’amiante au cours des opérations de construction, d’entretien et de démolition des bâtiments.

L’amiante est ou a été en général utilisé comme un mélange fibreux lié à d’autres matériaux

(par exemple du ciment, des plastiques ou des résines) ou sous forme tissée comme un

textile. Il a été employé dans une vaste gamme d’applications comportant les toitures, les

plaques de ciment pour les planchers et les murs, les canalisations en ciment (par exemple

pour l’alimentation en eau), l’isolation thermique et électrique, notamment les couvertures

antifeu et les rideaux pare-flammes dans l’industrie, les joints d’étanchéité et les matériaux de

friction (par exemple les sabots de frein et les garnitures de disques de frein et d’embrayage

dans les véhicules). De nos jours, l’exposition aux fibres d’amiante survient plus particulière-

ment dans les situations où les produits d’amiante ont été dégradés, par exemple pendant les

opérations d’entretien et de démolition des bâtiments, l’élimination des déchets, mais aussi

dans le contexte des catastrophes naturelles.

Pourquoi est-il si important de s’attaquer à l’amiante parmi tous les autres agents cancérogènes, alors que l’on en trouve tant d’autres dans l’environnement ?

On pense que certains cancers dus à des facteurs environnementaux ont de multiples déter-

minants. D’autres cependant trouvent leur cause dans des agents cancérogènes isolés et

identifiables, comme le tabac ou l’amiante, auxquels l’exposition est évitable. (Note : ce n’est

pas le cas pour de nombreux agents classés par le Centre international de Recherche sur

le Cancer [CIRC] dans le groupe 1, celui des agents cancérogènes pour l’homme ; nombre

d’entre eux n’entraînent pas non plus la même charge de morbidité.)1

L’une des raisons pour lesquelles il est important que les pays prennent le plus vite possible

des mesures contre l’amiante est liée à la période de latence particulièrement longue entre

l’exposition et l’apparition du mésothéliome, qui peut souvent atteindre 40 ans. Cela explique

que le fardeau des maladies liées à l’amiante continuera d’augmenter dans un premier temps,

même dans les pays qui en ont interdit l’usage il y a de nombreuses années.

1 Pour plus de détails sur les agents cancérogènes classés dans le groupe 1 par le CIRC, voir http://monographs.iarc.fr/ENG/Classification/ClassificationsGroupOrder.pdf.

On a des preuves scientifiques

indubitables que l’amiante provoque

des cancers et des maladies respiratoires

chroniques chez l’homme

http://monographs.iarc.fr/ENG/Classification/ClassificationsGroupOrder.pdf

http://monographs.iarc.fr/ENG/Classification/ClassificationsGroupOrder.pdf


Toutes les formes d’amiante peuvent provoquer le cancer chez l’homme (y compris le chryso-

tile, la principale forme encore produite et utilisée) et aucun seuil n’a été mis en évidence pour

le risque cancérogène. C’est la conclusion à laquelle l’OMS et le CIRC sont parvenus dans

une série d’évaluations internationales faisant autorité et menées sur une période de plus de

15 ans, la plus récente d’entre elles ayant été publiée par le CIRC en 2012. On retrouve dans

ces conclusions le consensus international d’experts scientifiques réunis par l’OMS pour éva-

luer les effets de l’amiante sur la santé.

De plus, on a montré que l’exposition concomitante à la fumée de tabac et à l’amiante

augmente considérablement le risque de cancer pulmonaire, avec un effet qui au moins s’ad-

ditionne, c’est-à-dire que plus la consommation de tabac augmente, plus le risque s’accroît.

Peut-on être certain que les évaluations scientifiques de l’amiante faites par l’OMS et le CIRC échappent totalement à toute influence extérieure ?

Oui. À chaque fois, des mesures ont été prises pour s’assurer que tout conflit d’intérêts poten-

tiel soit identifié et résolu, que les évaluations soient extrêmement rigoureuses et totalement

indépendantes des opinions des gouvernements, des institutions nationales et des groupes

d’intérêts spéciaux, que les opinions de toutes les régions du monde soient prises en compte

et qu’il y ait un examen collégial international approfondi.

Quelles mesures ont été prises par les pays au niveau national ?

De nombreux pays, plus de 50 États Membres de l’OMS (fin 2013), ont

déjà légiféré pour interdire l’utilisation de l’amiante afin de protéger et

de promouvoir la santé publique.2 En général, la décision a été prise

après consultation pangouvernementale pour tenir compte des intérêts

sectoriels, tout en évitant qu’ils ne prédominent trop dans la décision

finale. Au moment d’envisager des mesures législatives contre l’utilisa-

tion de l’amiante, il a été nécessaire de prendre en compte toute une

série de coûts et d’avantages, dont les coûts de prestation des services

de santé et ceux associés à la perte de productivité de la main d’œuvre

imputable aux maladies chroniques, en plus des considérations éco-

nomiques et commerciales classiques.

Quelles mesures ont été prises ou sont proposées par les pays à un niveau international ?

La Convention de Bâle sur le contrôle des mouvements transfrontières

de déchets dangereux et de leur élimination, qui est entrée en vigueur

en 1992 et à laquelle 181 pays sont Parties, vise à protéger la santé de

l’homme et l’environnement contre les effets indésirables des déchets

dangereux. L’amiante (poussières et fibres) est inscrite dans une caté-

gorie des déchets à contrôler au titre de la Convention. Les Parties à la

2 L’Afrique du Sud, l’Algérie, l’Arabie saoudite, l’Argentine, l’Australie, le Bahreïn, le Brunei Darussalam, le Chili, l’Égypte, le Gabon, le Honduras, l’Islande, Israël, le Japon, la Jordanie, le Koweït, le Mozambique, la Norvège, Oman, le Qatar, la République de Corée, la Serbie, les Seychelles, la Suisse, la Turquie, les 28 États Membres de l’Union européenne et l’Uruguay. L’amiante est également interdit dans deux États du Brésil : Rio de Janeiro et Rio Grande do Sul.


Convention sont tenues d’interdire ou de ne pas permettre l’exportation de ces déchets dans

les Parties qui en ont interdit l’importation au titre de la Convention.

Plus récemment, une majorité des 154 pays qui sont Parties à la Convention de Rotterdam

sur la procédure de consentement préalable en connaissance de cause applicable à cer-

tains produits chimiques et pesticides dangereux qui font l’objet du commerce international

(entrée en vigueur en 2004) a manifesté le souhait de voir le chrysotile inscrit à l’annexe III

de la Convention. Cela signifierait que le chrysotile serait alors soumis à la procédure impo-

sant à un pays de prendre une décision en toute connaissance de cause avant d’autoriser ou

non des importations de cette substance dans le futur. Jusqu’à présent toutefois, l’inscription

du chrysotile a été bloquée par un petit nombre de pays qui, en majorité mais pas exclusi-

vement, ont toujours un intérêt dans la commercialisation et l’utilisation du chrysotile et des

produits qui en contiennent.

Est-il vrai que le chrysotile est moins nocif que d’autres types d’amiante et qu’il ne devrait donc pas être soumis aux mêmes mesures de contrôle ?

Les données scientifiques sont sans équivoque. La ferme conclusion des évaluations de

l’OMS et du CIRC est que le chrysotile provoque des cancers du poumon, du larynx, de

l’ovaire, le mésothéliome et l’asbestose, qu’il soit ou non moins actif que les amphiboles à cet

égard. Les affirmations sur les différences de propriétés physicochimiques ou sur la question

de savoir si les études épidémiologiques dans les pays ont porté sur du chrysotile contaminé

par des amphiboles ou du chrysotile confiné dans les ciments modernes de haute densité (au

moment de la fabrication) ne changent rien à l’affaire.

Une inquiétude majeure est que, même quand l’utilisation est correctement réglementée,

les produits pour la construction contenant du chrysotile (tuiles de toit, canalisations par

exemple) se dégradent et libèrent des fibres d’amiante dans l’environnement au cours des

opérations d’entretien, de démolition des bâtiments et d’évacuation des déchets,

ou lors de catastrophes naturelles. Cette exposition peut survenir après l’ins-

tallation (contrôlée) à l’origine. On peut totalement éviter ce risque en cessant

d’utiliser ces produits. Les organisations nationales, régionales et internationales

ont à disposition des informations sur les matériaux et produits de remplacement

que l’on peut employer en toute sécurité.

Les travaux de recherche actuels ou futurs pourraient-ils modifier l’opinion actuelle de l’OMS et du CIRC concernant la survenue du cancer ?

Absolument pas : l’opinion ferme et définitive de l’OMS et du CIRC, sur la base

des évaluations répétées et des données scientifiques, est que le chrysotile pro-

voque des cancers du poumon, du larynx et de l’ovaire, le mésothéliome et

l’asbestose et que l’arrêt de l’utilisation de toutes les formes d’amiante, chryso-

tile compris, pour éviter l’exposition devrait être reconnu comme le moyen le plus

efficace d’éliminer les maladies liées à l’amiante. Bien qu’on ait clairement iden-

tifié le potentiel cancérogène du chrysotile, peu d’études ont inclus des femmes.

On soupçonne également que le chrysotile serait associé à d’autres cancers pour

lesquels les études qui existent sont insuffisantes. Il existe donc encore un besoin

La ferme conclusion des évaluations de

l’OMS et du CIRC est que le

chrysotile provoque des cancers du

poumon, du larynx, de l’ovaire,

le mésothéliome et l’asbestose


de mener de nouvelles recherches pour étudier les risques d’autres types de cancer en rap-

port avec l’exposition au chrysotile, en particulier pour ce qui est des cancers spécifiquement

féminins.

De quelles informations dispose-t-on sur les produits de remplacement, notamment pour les matériaux de construction, compte tenu des assertions selon lesquelles les fibres modernes de substitution du chrysotile sont toxiques ou ont une toxicité qui n’a pas été déterminée ?

De nombreux gouvernements nationaux, organismes régionaux et organisations interna-

tionales ont identifié des solutions de remplacement ou des substituts pour les usages de

l’amiante et des évaluations sanitaires des produits de substitution ont été publiées. Par

exemple, un atelier OMS/CIRC a été organisé en 2005 et le Gouvernement du Royaume-Uni,

la Commission européenne et le Bureau régional OMS de l’Europe ont fait des publica-

tions. Les évaluations des dangers des matériaux de substitution du chrysotile pour la santé

humaine se sont concentrées sur d’autres types de matières fibreuses en raison des risques

potentiels liés à l’inhalation des fibres. Il faut cependant noter que, pour certains usages, le

chrysotile peut être remplacé par des matières non fibreuses, par exemple du chlorure de

polyvinyle non plastifié (UPVC) ou du métal en feuilles.

L’absence de cas notifiés de mésothéliome dans un pays indique-t-elle qu’il n’y a pas de charge de morbidité significative due à l’amiante et qu’il n’y a donc pas de raison d’agir, vu la spécificité du mésothéliome en tant que marqueur de l’exposition à l’amiante ?

Non. La détection des cas de mésothéliome et l’établissement précis de leur nombre néces-

sitent l’existence de systèmes de surveillance systématique au niveau national alors que,

souvent, il n’y en a pas. Il faut également se souvenir que la période de latence entre l’exposi-

tion à l’amiante et l’apparition d’un mésothéliome peut atteindre 40 ans ou plus, de sorte que

ces systèmes doivent être en place sur une longue durée.

L’amiante a une probabilité plus grande de provoquer un cancer pulmonaire qu’un méso-

théliome (estimation du rapport des risques de 6/1) et la probabilité est également plus forte

chez le fumeur. Le cancer du poumon est beaucoup plus cou-

rant que le mésothéliome et a une origine multifactorielle. Il est

facile de perdre de vue des antécédents d’exposition à l’amiante

(y compris dans un milieu non professionnel, voir ci-après) qui

se sont produits de nombreuses années auparavant. L’absence

d’éléments probants au niveau national pour le moment n’est

pas une preuve de l’absence du problème et il faut tenir compte

des enseignements que l’on peut tirer de l’expérience d’autres

pays où de grandes épidémies de mésothéliome surviennent

encore, même après de nombreuses années après l’arrêt des

expositions généralisées à l’amiante.


L’exposition à l’amiante est-elle seulement un problème professionnel, avec peu ou pas de risque pour la population en général ?

Non. De nombreux cas de mésothéliome ont été décrits chez les épouses et les enfants d’ou-

vriers travaillant l’amiante, suite à une exposition domestique (au moins 376 cas), chez les

cols blancs dans le secteur de l’amiante et chez les personnes vivant à proximité des mines

à cause de la pollution de l’air ; on a aussi signalé des cas d’asbestose chez les épouses et

les enfants des ouvriers travaillant l’amiante. On a décrit des cas de mésothéliome chez des

sujets exposés à l’amiante naturel ou à des minéraux de ce type présents dans les sols de

régions en Turquie, en Grèce, à Chypre, en Corse, en Sicile, en Nouvelle-Calédonie, dans la

province du Yunnan en Chine et en Californie. Bien que ce dernier groupe ne puisse être

protégé par des mesures de contrôle de la production et de l’utilisation de l’amiante, celles-ci

seront utiles pour les autres groupes.

On observe d’autres types d’exposition dans l’environnement. Des rapports en provenance

d’Australie et du Royaume-Uni ont indiqué qu’il y avait aux intersections où la circulation est

dense une élévation des concentrations de fibres d’amiante imputable à la présence des maté-

riaux de friction dans les véhicules. Les expositions en milieu non professionnel proviennent

des opérations de rénovation des domiciles et d’entretien des voitures. En plus de l’exposition

professionnelle des ouvriers du bâtiment (les mesures de lutte contre l’exposition à l’amiante

étant difficiles à mettre en place pour une main-d’œuvre nombreuse, fragmentée et pouvant

comporter de nombreux travailleurs non déclarés), il y a aussi potentiellement une exposi-

tion en dehors du cadre professionnel aux déchets de construction contenant de l’amiante si

ceux-ci ne sont pas entreposés et éliminés correctement. Entre aussi dans cette catégorie le

risque de récupération et de réutilisation de ces déchets pour les habitations de fortune.

La préoccupation des responsables politiques aujourd’hui concerne moins l’exposition pro-

fessionnelle dans les secteurs de l’exploitation minière et de la fabrication de l’amiante que

l’utilisation de matériaux qui en contiennent dans le secteur du bâtiment. Les inquiétudes

portent sur l’exposition professionnelle pendant les activités de construction et celles sur-

venant par inadvertance dans l’ensemble de la population à cause de la dégradation des

matériaux de construction (par exemple des tuiles ondulées d’amiante cassées) et de l’éva-

cuation inappropriée des déchets. L’utilisation de matériaux de construction renfermant de

l’amiante dans les communautés les plus pauvres, qui met les familles à proximité immé-

diate des sources d’exposition aux fibres de chrysotile, est à cet égard particulièrement

préoccupante.

Il y a potentiellement

une exposition en dehors du cadre

professionnel aux déchets de

construction contenant de

l’amiante


Informations complémentairesAutres publications de l’OMS sur l’amiante

Titre Description Site Web

Projet pour l’élaboration de programmes nationaux pour l’élimination des maladies liées à l’amiante. Organisation internationale du Travail et Organisation mondiale de la Santé ; 2007

Ce document, à l’intention des pays, vise à leur faciliter la création de leurs programmes nationaux pour l’élimination des maladies liées à l’amiante. Il s’intéresse aussi à leurs efforts de prévention des maladies liées à l’amiante, résultat de l’exposition aux diverses formes d’amiante déjà en place ou résultant de leur utilisation dans le passé. Disponible en anglais, arabe, chinois, espagnol, français et russe.

http://www.who.int/occupational_health/publications/elim_asbestos_doc_fr.pdf?ua=1, consulté le 11 mars 2014

Asbestos – hazards and safe practices for clean up after earthquake. Organisation mondiale de la Santé ; 2008

Ce document donne des indications sur la manière de maîtriser les risques liés à l’amiante au cours des opérations de nettoyage et d’évacuation des déchets contenant de l’amiante provenant de bâtiments endommagés ou détruits à la suite de tremblements de terre ou d’autres catastrophes naturelles.

http://www.who.int/hac/crises/chn/asbestos/en/, consulté le 11 mars 2014

Évaluations publiées sur les matériaux de substitution

Titre Description Site Web

Review of substitutes for asbestos construction products by a WHO temporary advisor. Dans : National programmes for elimination of asbestos-related diseases: review and assessment. Bureau régional OMS de l’Europe ; 2012 : annexe 4

Examen de la disponibilité et de l’innocuité des matériaux de substitution de l’amiante, qui est un document de fond rédigé par un conseiller temporaire de l’OMS pour une réunion sur la lutte contre l’amiante organisée par la Région européenne de l’OMS. Disponible en anglais et en russe.

http://www.euro.who.int/en/health-topics/environment-and-health/occupational-health/publications/2012/national-programmes-for-elimination-of-asbestos-related-diseases-review-and-assessment, consulté le 11 mars 2014

Opinion on chrysotile asbestos and candidate substitutes. Comité scientifique de la toxicité, de l’écotoxicité et de l’environnement (CSTEE), Commission européenne ; 1998

Évaluation des risques pour la santé humaine posés par trois fibres de substitution – fibres de cellulose, fibres de PVA et fibres de p-aramide – par un comité d’experts de la Commission européenne.

http://ec.europa.eu/health/scientific_committees/environmental_risks/opinions/sctee/sct_out17_en.htm, consulté le 11 mars 2014

Harrison et al. Comparative hazards of chrysotile asbestos and its substitutes: a European perspective. Environ Health Perspect., 1999;107:607-11

Évaluation des matériaux de substitution de l’amiante préparée pour la Commission de la Santé et de la Sécurité du Royaume-Uni (Londres, Royaume-Uni), puis publiée dans la littérature scientifique.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566482/, consulté le 11 mars 2014

http://www.who.int/occupational_health/publications/elim_asbestos_doc_fr.pdf?ua=1



http://www.who.int/hac/crises/chn/asbestos/en/

http://www.who.int/hac/crises/chn/asbestos/en/

http://www.euro.who.int/en/health-topics/environment-and-health/occupational-health/publications/2012/national-programmes-for-elimination-of-asbestos-related-diseases-review-and-assessment






http://ec.europa.eu/health/scientific_committees/environmental_risks/opinions/sctee/sct_out17_en.htm



http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566482/

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566482/


Technical summary of WHO evaluations of chrysotile

Introduction ................................................14

Chrysotile production, use and exposure ..........15

Production ..................................................... 15

Use ............................................................... 15

Non-occupational exposure .............................. 16

Occupational exposure ..................................... 16

Health effects ..............................................20

Cancer of the lung ........................................... 20

Studies in experimental animals ................... 20

Studies in humans ..................................... 20

IARC conclusions on cancer of the lung ........ 23

Key new studies ........................................ 23

Mesothelioma ................................................. 26

Studies in experimental animals ................... 26

Studies in humans ..................................... 26

IARC conclusions on mesothelioma .............. 30

Key new studies ........................................ 30

Asbestosis ...................................................... 31

IPCS conclusions ....................................... 32

Global burden of disease .................................. 33

Cancer of the lung ..................................... 33

Mesothelioma ............................................ 33

Asbestosis ................................................ 33

Chrysotile substitute fibres ................................ 34

Methodological aspects .............................. 34

Hazard assessment .................................... 36

References .................................................40


IntroductionThis technical summary on the health effects of chrysotile summarizes the most recent author-

itative World Health Organization (WHO) evaluations performed by its International Agency for

Research on Cancer (IARC) and its International Programme on Chemical Safety (IPCS). Key

studies published after these evaluations are also briefly reviewed. The purpose of this techni-

cal summary is to assist policy-makers in assessing the importance of undertakings to prevent

the adverse health effects – cancer and lung fibrosis – associated with exposure to chrysotile.

WHO has conducted a number of evaluations of the health effects associated with exposure

to chrysotile over the past 20 years (1, 2). These evaluations have concluded that all forms of

asbestos, including chrysotile, are carcinogenic to humans, causing mesothelioma and can-

cer of the lung, larynx and ovary. Chrysotile also causes non-malignant lung diseases, which

result in deterioration of lung function (asbestosis). Many scientific studies linking domestic

and environmental exposure to asbestos with adverse health effects have also been identified,

alongside the large number of studies in occupational settings.

Most informative in the evaluation of the effects of chrysotile exposure in humans (1) have been

the studies performed in chrysotile mines in Quebec, Canada (most recent cohort update) (3), a chrysotile mine in Balangero, Italy (4, 5), cohorts of textile workers in South Carolina (6) and

North Carolina, United States of America (USA) (7), and two cohorts of asbestos factory work-

ers in China (8, 9). More recently, studies on chrysotile miners (10–12) and chrysotile textile

workers in China (13–17) and two meta-analyses (18, 19) have further consolidated the data-

base. All types of asbestos cause asbestosis, mesothelioma and cancer of the lung, larynx and

ovary (1, 2). This text concentrates on cancer of the lung, mesothelioma and asbestosis, as

these have been the principal areas of research until relatively recently.

“There is sufficient evidence in humans for the carcinogenicity of all forms of asbestos (chrysotile, crocidolite, amosite, tremolite, actinolite and anthophyllite). Asbestos causes mesothelioma and cancer of the lung, larynx and ovary.” (1)


Chrysotile production, use and exposureProductionChrysotile has always been the main asbestos species mined; in the peak year of production

(1979), chrysotile comprised more than 90% of all asbestos mined (20). With the excep-

tion of small amounts (approximately 0.2 Mt annually, in 2007–2011) of amphibole asbestos

mined in India, chrysotile is at present the only asbestos species mined. World production

in 2012 was estimated to be 2 Mt, the main producers being the Russian Federation (1 Mt),

China (0.44 Mt), Brazil (0.31 Mt) and Kazakhstan (0.24 Mt); production has stopped in

Canada, which until 2011 was one of the main producers. Although world production has

decreased considerably from its peak of 5.3 Mt in 1979, it has remained stable during the

2000s (2–2.2 Mt) (21–23).

Use

Asbestos is used as a loose fibrous mixture, bonded with other materials (e.g. Portland

cement, plastics and resins) or woven as a textile. The range of applications in which asbes-

tos has been used includes roofing, thermal and electrical insulation, cement pipe and sheets,

flooring, gaskets, friction materials (e.g. brake pads and shoes), coating and caulking com-

pounds, plastics, textiles, paper, mastics, thread, fibre jointing and millboard (1).

Organizations that track the usage of chrysotile globally report that all asbestos (including

chrysotile) use had been prohibited in 32 countries by 2007, rising to approximately 50

countries by 2014 (24). The form of prohibition in countries can vary (e.g. exemptions for lim-

ited, highly specialized engineering uses can be permitted), which complicates the process


of determining the status of a country at any given time. However, countries that have pro-

hibited all widespread and large-scale uses of all types of asbestos (including chrysotile)

include Algeria, Argentina, Australia, Bahrain, Brunei Darussalam, Chile, Egypt, the 28 mem-

ber states of the European Union, Gabon, Honduras, Iceland, Israel, Japan, Jordan, Kuwait,

Mozambique, Norway, Oman, Qatar, Republic of Korea, Saudi Arabia, Serbia, Seychelles,

South Africa, Switzerland, Turkey and Uruguay. Asbestos is also banned in two states of Brazil,

Rio de Janeiro and Rio Grande do Sul (25).

Although asbestos has not been banned in the USA, consumption decreased from

668 000 t in 1970 to 359 000 t in 1980, 32 t in 1990, 1.1 t in 2000 and 1.0 t in 2010 (22, 23). Consumption of asbestos (mainly chrysotile) was 143 000 t in the United Kingdom in

1976, decreasing to 10 000 t in 1995; as the use of asbestos is banned in the European

Union, it is expected to be zero at present. France imported approximately 176 000 t of asbes-

tos in 1976; imports stopped by 1996, when France banned asbestos use. In Germany, the

use of asbestos amounted to approximately 175 000 t annually from 1965 to 1975 and came

to an end in 1993. In Japan, asbestos consumption was approximately 320 000 t in 1988

and decreased steadily over the years to less than 5000 in 2005; asbestos use was banned

in 2012 (26). In Singapore, imports of raw asbestos (chrysotile only) decreased from 243 t

in 1997 to 0 t in 2001 (27). In the Philippines, the importation of raw asbestos was approxi-

mately 570 t in 1996 and 450 t in 2000 (28). However, in some countries, such as Belarus,

Bolivia (Plurinational State of), China, Ghana, India, Indonesia, Pakistan, Philippines, Sri

Lanka and Viet Nam, the use of chrysotile increased between 2000 and 2010. In India, use

increased from 145 000 t in 2000 to 462 000 t in 2010 (21, 23); in Indonesia, the increase

was from 45 045 t in 2001 to 121 548 t in 2011 (29).

Non-occupational exposureNon-occupational exposure, also loosely called environmental exposure, to asbestos may be

due to domestic exposure (e.g. living in the same household with someone exposed to asbes-

tos at work), air pollution from asbestos-related industries or the use of asbestos-containing

friction materials, or naturally occurring asbestos minerals.

In studies of asbestos concentrations in outdoor air, chrysotile is the predominant fibre

detected. Low levels of asbestos have been measured in outdoor air in rural locations (typ-

ical concentration, 10 fibres/m3).3 Typical concentrations are about 10-fold higher in urban

locations and about 1000 times higher in close proximity to industrial sources of exposure.

Elevated levels of chrysotile fibres have also been detected at busy traffic intersections, pre-

sumably from braking vehicles (30). In indoor air (e.g. in homes, schools and other buildings),

measured concentrations of asbestos are in the range of 30–6000 fibres/m3 (1).

Occupational exposureExposure by inhalation and, to a lesser extent, ingestion occurs in the mining and milling

of asbestos (or other minerals contaminated with asbestos), the manufacturing or use of

products containing asbestos, and the construction, automotive and asbestos abatement

industries (including the transport and disposal of asbestos-containing wastes) (1). In esti-

mates published in 1998, when most European Union countries had already banned the

3 1 fibre/m3 = 1 × 10−6 fibres/mL; 1 fibre/mL = 1 × 106 fibres/m3.


use of all asbestos, it was estimated that the proportion of the European Union workforce

still exposed to asbestos (mainly chrysotile) in different economic subsectors (as defined by

the United Nations) (31) was as follows: agriculture, 1.2%; mining, 10.2%; manufacturing,

0.59%; electrical, 1.7%; construction, 5.2%; trade, 0.3%; transport, 0.7%; finance, 0.016%;

and services, 0.28% (32, 33).

In 2004, it was estimated that 125 million people were exposed to asbestos (as stated above,

mainly to chrysotile) at work (34).

The National Institute for Occupational Safety and Health (NIOSH) in the USA estimated in

2002 that 44 000 miners and other mine workers may have been exposed to asbestos dur-

ing the mining of asbestos and some mineral commodities in which asbestos may have been

a potential contaminant. In 2008, the Occupational Safety and Health Administration (OSHA)

in the USA estimated that 1.3 million employees in construction and general industry face

significant asbestos exposure on the job (1). In Europe, based on occupational exposure to

known and suspected carcinogens collected during 1990–1993, the CAREX (CARcinogen

EXposure) database estimates that a total of 1.2 million workers were exposed to asbestos in

41 industries in the (then 15) member states of the European Union. Over 96% of these work-

ers were employed in the following 15 industries: “construction”, “personal and household

Elevated levels of chrysotile fibres have been detected at busy traffic intersections, presumably from braking vehicles


services”, “other mining”, “agriculture”, “wholesale and retail trade and restaurants and

hotels”, “food manufacturing”, “land transport”, “manufacture of industrial chemicals”,

“fishing”, “electricity, gas and steam”, “water transport”, “manufacture of other chemical

products”, “manufacture of transport equipment”, “sanitary and similar services” and “man-

ufacture of machinery, except electrical” (1). According to an unpublished report, in China,

120 000 workers of 31 asbestos mines come in direct contact with asbestos, and 1.2 million

workers are involved in the production of chrysotile asbestos products (35). Another unpub-

lished report indicated that in 31 asbestos factories in China with 120 000 workers, all these

workers could have come in contact with asbestos either directly or indirectly (35). In India,

approximately 100 000 workers in both organized and unorganized sectors were estimated

to be exposed to asbestos directly, and 30 million construction workers were estimated to be

subjected to asbestos dust on a daily basis (36). The number of exposed workers in Brazil

was estimated to be 300 000 (25).

In Germany, there was a steady decline in asbestos exposure between 1950 and 1990; the

90th percentile of the fibre count was between 0.5 and 1 fibre/mL in textile, paper/seals,

cement, brake pad and drilling/sawing activities in 1990 (37).

In France, median asbestos concentrations were highest in the building (0.85 fibre/mL in

1986–1996 and 0.063 fibre/mL in 1997–2004), chemical industry (0.34 and 0.1 fibre/mL,

respectively) and services (0.07 and 0.1 fibre/mL, respectively) sectors (38).

In 1999, the median asbestos (almost exclusively chrysotile) fibre counts in the air, as mea-

sured by personal samplers, in a Chinese asbestos textile plant were 6.5, 12.6, 4.5, 2.8 and

0.1 fibre/mL in the raw material (opening), raw material (bagging), textile, rubber plate and

asbestos cement sections of the plant; in 2002, the median asbestos fibre counts were 4.5,

8.6 and 1.5 fibres/mL in the raw material, textile and rubber plate parts of the plant (15).

In 2006, the geometric mean asbestos fibre count in the air in the largest chrysotile mine in

China was 29 fibres/mL, as estimated from gravimetric dust measurements. Available data

indicated that up to 1995, dust concentrations had been 1.5–9 times higher (11).

The geometric mean occupational exposures to asbestos fibres were 0.40, 1.70 and 6.70

fibres/mL in the construction, asbestos friction and asbestos textile industries in 1984 in the

Republic of Korea; in 1996, the corresponding figures were 0.14, 0.55 and 1.87 fibres/mL

(39). Park and colleagues (40) analysed 2089 asbestos exposure data sets compiled from

1995 through 2006 from 84 occupational sites. Asbestos exposure levels decreased from

0.92 fibre/mL in 1996 to 0.06 fibre/mL in 1999, possibly in part because of enforcement of

1997 legislation banning the use of amosite and crocidolite. During the periods 2001–2003

and 2004–2006, mean asbestos exposure levels declined further to 0.05 and 0.03 fibre/mL,

respectively. The mean concentration in the major primary asbestos production plants was

0.31 fibre/mL, and in the secondary asbestos industries (handlers and end uses of asbes-

tos-containing materials), 0.05 fibre/mL. In particular, a substantial reduction in asbestos

exposure levels was evident among primary industries handling raw asbestos directly. In this

industry, exposure dropped from 0.78 fibre/mL (period 1995–1997) to 0.02 fibre/mL (period

2003–2006).

In Thailand, breathing zone asbestos concentrations in 1987 in roof tile, cement pipe, vinyl

floor tile, asphalt undercoat and acrylic paint plants and in brake and clutch shops were

< 1.11, 0.12–2.13, < 0.18, < 0.06 and 0.01–58.46 fibres/mL, respectively. The brake and

In 2004, it was estimated that 125 million people were exposed to asbestos at work


clutch shops were small-scale enterprises, in contrast to the others; they had high asbestos

air concentrations also in 2000 (0.24–43.31 and 0.62–2.41 fibres/mL for the brake and clutch

shops, respectively) (41).

The occupational exposure limit for chrysotile has been lowered in the USA since the 1970s:

from 12 fibres/mL in 1971 to 5 fibres/mL in 1972, 2 fibres/mL in 1976, 0.2 fibre/mL in

1986 and 0.1 fibre/mL in 1994 (42). The occupational exposure limit for all asbestos spe-

cies is also 0.1 fibre/mL in the Bolivarian Republic of Venezuela (43), the European Union

(44), India (36), Indonesia (45), Malaysia (46), Norway (47), the Republic of Korea (39), Singapore (27) and the provinces of Alberta and British Columbia in Canada (48). Other occu-

pational exposure limits for all asbestos fibres include 0.01 fibre/mL in the Netherlands (49); 0.15 fibre/mL in Japan (26); 0.2 fibre/mL in South Africa (50); 0.8 fibre/mL in China (11, 35); and 2 fibres/mL in Brazil (48) and the Philippines (28). In Thailand, the labour law sets the

limit for airborne asbestos at 5 fibres/mL (41, 45). In Canada, the occupational exposure limit

for chrysotile is 1 fibre/mL (51).


Health effectsThe key studies on the main health end-points associated with exposure to chrysotile have

been summarized in Table 1 (see page 39).

Cancer of the lung

Studies in experimental animals

Bronchial carcinomas were observed in many experiments in rats after inhalation exposure to

chrysotile fibres. There was no consistent increase in tumour incidence at other sites (except

mesothelioma, see below) (1).

Studies in humans

Occupational exposure

In the final report on male workers in chrysotile mines in Quebec, Canada (3), there was an

exposure-related increase in mortality from lung cancer, reaching a standardized mortality

ratio (SMR) of 2.97 (95% confidence interval [CI]: 2.18–3.95) in the most heavily exposed

group. There was little difference between workers in the Asbestos and Thetford Mines areas

of Quebec; in the latter area, the chrysotile was (to a small extent) contaminated with tremolite.

An elevated mortality from lung cancer (SMR: 1.49; 95% CI: 1.17–1.87) was observed in a

cohort of chrysotile friction product plant workers in Connecticut, USA. Some anthophyllite

was used in some product lines during the last 20 years of the follow-up (52).

The risk of lung cancer was greatly increased among asbestos textile workers, mainly exposed

to chrysotile, who received compensation for work-induced asbestosis in Italy (SMR: 6.82;

95% CI: 3.12–12.95). There was no quantitative estimation of what the exposure to “mainly

chrysotile” represented (53).


Among workers with at least 1 year’s work experience between 1946 and 1987 in a chrysotile

mine in Balangero, northern Italy, the lung cancer SMR was 1.27 (95% CI: 0.93–1.70) dur-

ing the follow-up to 2003 (5). No fibrous amphiboles were found, but 0.2–0.5% of a fibrous

silicate, balangeroite, was identified in the chrysotile mined (54).

Among workers of eight chrysotile asbestos factories in China with at least 15 years of work

experience and followed from 1972 to 1986, the mortality from lung cancer was elevated (rel-

ative risk [RR]: 5.3; 95% CI: 2.5–7.1). The lung cancer risk was especially high among heavy

smokers (chrysotile-exposed non-smokers: RR: 3.8 [95% CI: 2.1–6.3]; chrysotile-exposed

light smokers: RR: 11.3 [95% CI: 4.3–30.2]; chrysotile-exposed medium smokers: RR: 13.7

[95% CI: 6.9–24.6]; chrysotile-exposed heavy smokers: RR: 17.8 [95% CI: 9.2–31.3]) (8).

In a study in an asbestos textile plant in South Carolina, USA, the exposure was almost exclu-

sively to chrysotile (part of the time, approximately 0.03% of the total amount of fibre used was

crocidolite, which was never carded, spun or twisted and was woven wet). The lung cancer

SMR was 1.95, with a 95% CI of 1.68–2.24. Exposure–response modelling for lung can-

cer, using a linear relative risk model, produced a slope coefficient of 0.0198 fibre-years/mL4

(standard error 0.004 96) when cumulative exposure was lagged 10 years (6).

In a cohort study in four asbestos textile mills in North Carolina, USA, workers with at least 1

day’s work between 1950 and 1973 were followed for mortality to 2003. In one of the plants,

a small amount of amosite was used between 1963 and 1976, whereas the others used

exclusively chrysotile (7). In subsequent analysis of fibres from North Carolina and South

Carolina by transmission electron microscopy, 0.04% of the fibres were identified as amphi-

boles (55). Lung cancer mortality was elevated in an exposure-related fashion and reached

an SMR of 2.50 (95% CI: 1.60–3.72) in the high-exposure category. The risk of lung cancer

increased with cumulative fibre exposure (rate ratio: 1.102 per 100 fibre-years/mL, 95% CI:

1.044–1.164, for total career exposure) (7).

Non-occupational exposure

There are few studies on lung cancer in people with non-occupational exposure to asbestos

and even fewer in which chrysotile specifically has been investigated.

In a cohort of 1964 wives (not working in the asbestos mills) of asbestos cement workers in

Casale Monferrato, Italy, the risk of dying from lung cancer was slightly elevated (SMR: 1.50;

95% CI: 0.55–3.26). The asbestos used was mainly chrysotile, but included approximately

10% crocidolite (56). A slightly elevated lung cancer risk was observed among spouses of

workers in an amosite factory in New Jersey, USA (SMR for male spouses of workers with

more than 20 years of exposure, 1.97 [95% CI: 1.12–3.44], and for female spouses of work-

ers with more than 20 years of exposure, 1.70 [95% CI: 0.73–3.36]) (57).

Meta-analyses

In an informal meta-analysis of 13 studies with dose–response information available in 1986,

WHO estimated the risk of lung cancer and mesothelioma in asbestos-exposed smokers and

non-smokers (58). Most of these studies have since been updated, new studies have become

available and formal meta-analyses of studies on lung cancer among chrysotile-exposed

workers have been performed, with the main aim to investigate the carcinogenic potency of

4 Cumulative exposure is expressed in units of (fibres/mL) × years. These units are given hereafter as fibre-years/mL.

Elevated mortality from lung cancer has been observed in chrysotile mine workers, chrysotile friction product plant workers and textile mill workers exposed to chrysotile


chrysotile, especially in comparison with that of amphibole asbestos species. Another objec-

tive of the meta-analyses has been the elucidation of possible differences in the carcinogenic

potency of fibres of different dimensions (i.e. length and thickness).

Lash et al. (59) conducted a meta-analysis based on the findings from 22 published studies

on 15 asbestos-exposed cohorts with quantitative information on asbestos exposure and lung

cancer mortality. Substantial heterogeneity was found in the slopes for lung cancer between

these studies. The heterogeneity was largely explained by industry category (mining and

milling, cement and cement products, or manufacturing and textile products), considered

to reflect the stages of asbestos fibre refinement, dose measurements, tobacco habits and

standardization procedures. There was no evidence that differences in fibre type (predomi-

nantly chrysotile, chrysotile mixed with other, or other) would explain the heterogeneity of the

slope – in other words, there was no difference in the potency to cause lung cancer between

the different fibre types.

Hodgson & Darnton (60) performed a meta-analysis based on 17 cohort studies with infor-

mation on the level of asbestos exposure. Marked heterogeneity was observed in the potency

slope derived from different chrysotile-exposed cohorts; the risk estimated from the South

Carolina, USA, asbestos textile plants (approximately 6% per fibre-year/mL) was similar to

the average in the amosite-exposed cohorts (5% per fibre-year/mL), whereas that from the

Quebec, Canada, mine studies was only 0.06% per fibre-year/mL, and the studies in asbestos

cement and friction product plants were intermediate in risk. Hodgson & Darnton (60) decided

to exclude the South Carolina study from the calculation, mainly because the risk derived for

the cohorts with mixed exposure (chrysotile + amphibole) was approximately 10% of that with

pure amphibole exposures, and concluded that the potency of chrysotile to cause lung can-

cer was 2–10% of that of the amphiboles. Their “best estimate” for excess lung cancer from

exposure to pure chrysotile was 0.1% per fibre-year/mL. However, the IARC Working Group

(1) noted that there is no justification for exclusion of the South Carolina cohort, because it is

one of the highest-quality studies in terms of the exposure information used in the study. An

alternative explanation of the large difference in the risk estimates from the mining studies and

the asbestos textile studies (also observed in the meta-analysis of Lash et al. (59)) could be

the differences in fibre dimensions: a larger percentage of long fibres was found in samples

from the South Carolina cohort (61) compared with what was previously reported in samples

from the Quebec mines and mills (62). A further possible cause of the difference is the differ-

ence in the quality of the exposure data (18).

Berman & Crump (63, 64) published a meta-analysis that included data from 15 asbestos

cohort studies. Lung cancer risk potency factors, based on a linear exposure–cancer risk rela-

tionship, were derived for fibre type (chrysotile versus amphiboles) and fibre size (length and

width).

As with the previous analyses, substantial variation was found in these studies, with results

for lung cancer varying by 2 orders of magnitude. The slope factor for chrysotile was

0.000 29 (fibre-year/mL)−1 for Quebec mining and 0.018 (fibre-year/mL)−1 for the South

Carolina textile workers. That for tremolite (vermiculite mines and milling operations in

Libby, Montana, USA) was 0.0026 (fibre-year/mL)−1, with an upper uncertainty level of 0.03

(fibre-year/mL)−1 , and that for amosite insulation, 0.024 (fibre-year/mL)−1 (64).


In a further analysis of the fibre dimensions, the hypothesis that long chrysotile fibres are

equipotent to long amphibole fibres was rejected for thin fibres (width < 0.2 μm), but not for

fibres of all widths or for thick fibres (width > 0.2 μm). When the South Carolina cohort was

dropped in a sensitivity analysis, the potency in the remaining studies in the meta-analysis

was significantly greater for amphiboles than for chrysotile (P = 0.005). Dropping the Quebec

cohort resulted in there being no evidence of a significant difference in potency between the

fibre types (P = 0.51) (63).

The IARC Working Group (1) noted that both the Hodgson & Darnton (60) and Berman &

Crump (63, 64) analyses reveal a large degree of heterogeneity in the study findings for lung

cancer and that findings are highly sensitive to the inclusion or exclusion of the studies from

South Carolina or Quebec. The reasons for the heterogeneity are unknown; until they are

explained, it is not possible to draw firm conclusions concerning the relative potency of chry-

sotile and amphibole asbestos fibres.

IARC conclusions on cancer of the lung

In respect of cancer of the lung, IARC concluded that there is sufficient evidence of carcino-

genicity in humans for all types of asbestos, including chrysotile. This is the strongest IARC

category for describing the strength of evidence (1).

Key new studies

Hodgson & Darnton (65) updated their meta-analysis of the lung cancer and mesothelioma

risks from exposure to different asbestos species following the publication of data for the North

Carolina, USA, chrysotile textile workers and noted that their original “best estimate”, 0.1%

It is not possible to draw firm conclusions concerning the relative potency of chrysotile and amphibole asbestos fibres


per fibre-year/mL, was practically identical to the estimate from the North Carolina cohort (RR:

1.102 per 100 fibre-years/mL).

In a cohort study in the largest chrysotile mine in Quinghai, China, all male workers (n = 1539)

employed at the beginning of 1981 were followed until the end of 2006. Mortality from dif-

ferent causes was compared with the national rates. Using a method with a sensitivity of

0.001%, no amphiboles were detected in the ore. The fibre exposure (estimated from gravi-

metric dust measurements in 2006) was 2.9–63.8 fibres/mL. The SMR for lung cancer was

4.71 (95% CI: 3.57–6.21). The SMR for the non-smoking chrysotile-exposed workers (min-

ers and millers) was 1.79 (95% CI: 0.49–6.51), and that for the non-smoking referents (rear

services and administration), 1.05 (95% CI: 0.19–5.96). For the smoking miners/millers, the

SMR was 5.45 (95% CI: 4.11–7.22), and for the smoking referents, 1.66 (95% CI: 0.71–3.88)

(11). Lung cancer mortality increased with increasing estimated fibre exposure, and the SMR

was 1.10 (95% CI: 0.47–2.28), 4.41 (95% CI: 2.52–7.71), 10.88 (95% CI: 6.70–17.68) and

18.69 (95% CI: 12.10–28.87) in the groups with estimated cumulative exposures of < 20,

20–100, > 100–450 and > 450 fibre-years/mL, respectively (12). In an overlapping study of

all 1932 workers employed for at least half a year between 1981 and 1988 and followed until

2010, the lung cancer SMR among the group considered directly exposed was 2.50 (95%

CI: 1.85–3.24) (10).

In the largest chrysotile factory in China, situated in Chongqing, in a follow-up of 584 male

workers for 37 years, the SMR for lung cancer was 4.08 (95% CI: 3.12–5.33) (14, 15). The

risk increased with estimated exposure and was seen in both non-smokers and smokers. In

females (n = 277), with a total employment time of only 19 years, a statistically non-signif-

icant excess of lung cancer was observed (SMR: 1.23; 95% CI: 0.34–4.50). The chrysotile

used in the factory was from a single source in China, and the content of tremolite was less


than 0.001% (66). An RR of 1.23 (95% CI: 1.10–1.38) per 100 fibre-years/mL was estimated

by fitting a log- linear model with a 10-year exposure lag (67).

In 2011, Lenters and co-workers (18) analysed the association of the quality of exposure

assessment with the estimated lung cancer potency of asbestos exposure in a meta-analysis

of 18 industrial cohorts and 1 population-based case–referent study. Stratification by exposure

assessment characteristics revealed that studies with well documented exposure assessment,

larger contrast in exposure, greater coverage of the exposure history by exposure measure-

ment data and more complete job histories had higher potency slope values than did studies

without these characteristics. Differences in potency for chrysotile compared with amphibole

asbestos were less evident when the meta-analysis was restricted to studies with higher-qual-

ity exposure data (18).

In order to better evaluate the carcinogenic potency of asbestos fibres at low exposure lev-

els, van der Bij and collaborators (19) applied, in addition to linear dose–exposure models,

a spline function to the lung cancer and exposure data from the studies with no fewer than

two risk estimates at different exposure levels. The spline function has the advantage that

responses at high exposures do not excessively determine the dose–response relationships

at low exposure levels. They found that in exposure to chrysotile alone, the relative lung can-

cer risks at lifetime exposures to 4 and 40 fibre-years/mL were 1.006 and 1.064, respectively

(natural spline function with correction for intercept). After stratification by fibre type, a non-

significant 3- to 4-fold difference in RRs between chrysotile and amphibole fibres was found

for exposures below 40 fibre-years/mL. The difference in potency between chrysotile and

amphiboles thus was considerably smaller than in the earlier analyses (60, 63). As in the other

meta-analyses, risk estimates for chrysotile were very different for the South Carolina, USA,

and Quebec, Canada, studies.


Kumagai and coworkers (68) assessed the relationship between lung cancer mortality and

asbestos exposure in the vicinity of an asbestos factory, based on meteorological modelling

of the town of Hashima, Japan, where an amosite–chrysotile plant operated in 1943–1991.

Excluding individuals with occupational exposure to asbestos or silica, lung cancer risk was

elevated among those with highest estimated environmental asbestos exposure (SMR: 3.5;

95% CI: 1.52–5.47).

The standardized incidence ratio (SIR) for lung cancer during a 10-year period in 15 vil-

lages in Turkey with environmental asbestos exposure was 1.82 (95% CI: 1.42–2.22) in men

and 1.80 (95% CI: 1.43–2.00) in women, in comparison with 12 villages with no asbestos

exposure. The estimated lifetime asbestos exposure range was 0.19–4.61 fibre-years/mL;

the fibre type was either tremolite or a mixture of tremolite + actinolite + chrysotile or antho-

phyllite + chrysotile. Lung cancer risk was elevated in both non-smokers (SIR: 6.87; 95% CI:

3.58–13.20) and smokers (SIR: 12.50; 95% CI: 7.54–20.74) (69).

Mesothelioma

Studies in experimental animals

After intrapleural or intraperitoneal injection of chrysotile, mesothelioma induction was con-

sistently observed in rats, when samples contained a sufficient number of fibres with a fibre

length of greater than 5 μm. In several studies in rats, mesotheliomas were also observed after

inhalation exposure to chrysotile (1).

Studies in humans

Occupational exposure

An excess of mesothelioma has been reported in cohort studies of chrysotile-exposed miners

and millers (38 cases out of a total of 6161 deaths) in Quebec, Canada (3), and of asbestos

textile workers (3 cases out of 1961 deaths) in South Carolina, USA, who were predominantly

exposed to chrysotile asbestos imported from Quebec (6). However, the fact that chrysotile

mined in Quebec is contaminated with a small percentage (< 1%) of amphibole asbestos

(tremolite) complicates the interpretation of these findings. McDonald et al. (70) found that in

the Quebec mining areas, the mortality from mesothelioma was 3 times higher among workers

from mines in Thetford Mines, a region with higher concentrations of tremolite, than among

those from mines in Asbestos, with lower concentrations of tremolite. However, Begin et al.

(71) noted that although tremolite levels may be 7.5 times higher in Thetford Mines than in

Asbestos, the rate of mesothelioma in the asbestos mine/mill workforce of these two towns

was similar. This does not support the notion that the tremolite content of the ores is the deter-

minant of mesothelioma risk in Quebec chrysotile workers.

No cases of mesothelioma among the total of 803 deaths were observed in the Connecticut,

USA, friction material plant workers exposed to chrysotile (52).

There were two cases of malignant pleural tumours among asbestos textile workers who

received compensation for work-induced asbestosis in Italy; this represents a greatly increased

risk (SMR: 22.86; 95% CI: 2.78–82.57). There was a more pronounced increase in the risk

of peritoneal tumours. The exposure was described as “mainly chrysotile”, but no quantita-

tive data on the exposure were provided (53).

Malignant mesothelioma has been linked to occupational, domestic and environmental exposure to asbestos


Among 126 cases of mesothelioma identified in six referral hospitals in South Africa, 23 cases

had mined Cape crocidolite; 3 had mined amosite; and 3, crocidolite plus amosite. None had

purely chrysotile exposure (72). It should be noted that chrysotile mining began later, and pro-

duction levels were lower than in the crocidolite and amosite mines of South Africa.

Cases of mesothelioma have been reported among asbestos miners in Zimbabwe (73). Chrysotile from Zimbabwe has been reported to contain 3 orders of magnitude less tremolite

than that from Thetford Mines, Quebec (74).

Asbestos textile workers in North Carolina, USA, were primarily exposed to chrysotile

imported from Quebec, Canada. Large excesses of both mesothelioma (SMR: 10.92; 95% CI:

2.98–27.96) and pleural cancer (SMR: 12.43; 95% CI: 3.39–31.83) were observed (7).

Two cases of mesothelioma were observed in the 1990 study in the Balangero, Italy, chrysotile

mine (54). However, in a follow-up until 2003, four pleural and one abdominal mesothelioma

were identified, giving SMRs of 4.67 (95% CI: 1.27–11.96) for pleural mesothelioma and 3.16

(95% CI: 1.02–7.36) for all mesothelioma (5).

Non-occupational exposure

Since the first large case-series published by Wagner and co-workers (75) linking malignant

mesothelioma to occupational, domestic and environmental exposure to asbestos, at least 376

cases of mesothelioma for which domestic exposure to asbestos has been considered the caus-

ative agent have been published in some 60 scientific papers (76).


Three cases of mesothelioma were identified in 1980–2006 from the mesothelioma registry in

Piedmont, northern Italy, among white collar workers of the Balangero chrysotile mine, three

among employees of a subcontractor working as lorry drivers in the mine, four among per-

sons living in the vicinity of the mine, one the wife of a mine worker and five cases who had

had contact with the main tailings (4). No fibrous amphiboles were found, but 0.2–0.5% of a

fibrous silicate, balangeroite, was identified in the chrysotile mined in Balangero (54).

In a cohort of 1780 wives (not working in the asbestos mills) of asbestos cement workers in

Casale Monferrato, Italy, the risk of dying from malignant pleural tumours was elevated in

1965–2003 (SMR: 18.00; 95% CI: 11.14–27.52). The asbestos used was mainly chrysotile,

but included approximately 10% crocidolite (56, 77). The incidence of histologically verified

pleural mesothelioma in 1999–2001 was also elevated in a roughly latency- and exposure

duration–dependent way, reaching an SIR of 50.59 (95% CI: 13.78–129.53) in the group with

a latency of at least 40 years and duration of exposure of at least 20 years.

In a population-based case–referent study in a local health area of Casale Monferrato, Italy, the

association between non-occupational asbestos exposure and malignant mesothelioma was

examined for 116 cases of mesothelioma diagnosed in 1987–1993 and 330 referents. The

odds ratio (OR) for the cases to be a spouse of an asbestos worker was 4.5 (95% CI: 1.8–11.1);

the OR for the cases to be a child of an asbestos worker was 7.4 (95% CI: 1.9–28.1). The risk

was inversely related to the distance between the residence and the asbestos factory, reach-

ing an OR of 27.7 (95% CI: 3.1–247.7) for those ever living less than 500 m from the factory.

In 1984, the average asbestos concentrations in the air were reported to be 0.011 fibre/mL

close to the plant and 0.001 fibre/mL in the residential area. In different studies, the propor-

tion of amphiboles varied between 3% and 50% of total asbestos fibres (78).

Of the 162 female cases of fatal mesothelioma in Canada and the USA in 1966–1972, three

occurred in wives of workers in Quebec chrysotile mines (79). In a case–referent study among

wives of workers in Quebec chrysotile mines, the risk of living with a mine worker for less than

40 years was associated with a mesothelioma risk of 3.9 (95% CI: 0.4–35); the risk of living

with a mine worker for more than 40 years was associated with a risk of 7.5 (95% CI: 0.8–72).

All cases had lived with a worker from the mine in Thetford Mines, where the chrysotile ore

was contaminated with tremolite (80).

In several countries or regions in different parts of the world – Turkey, Greece, Cyprus, Corsica,

Sicily, New Caledonia, Yunnan province, China, and California, USA – there are areas with

a high incidence of mesothelioma, apparently caused by asbestos or erionite in soil (1, 81).

In a case–referent study of 1133 mesothelioma cases and 890 referents in California, the risk

of mesothelioma was observed to be inversely related to the distance of the residence from

naturally occurring asbestos ultramafic rocks, which contain serpentinic asbestos. The meso-

thelioma risk decreased with an SMR of 0.937 (95% CI: 0.895–0.982) per 10 km of distance,

adjusted for age and probability of occupational asbestos exposure (82).

In a case–referent study of 68 cases of mesothelioma in New Caledonia, the prevalence of

mesothelioma in different parts of the island was related to the serpentinite content of the soil,

not to mining activity or the use of the traditional lime, “pö”, to cover houses (83).


Meta-analyses

From a meta-analysis of cohort studies with quantitative information on exposure, Hodgson

& Darnton (60) estimated that the excess mesothelioma risk was 0.1% per fibre-year/mL for

cohorts exposed to chrysotile.

The meta-analysis conducted by Berman & Crump (64) was based on the analysis of the

slopes that were estimated assuming that the mortality rate from mesothelioma increases after

exposure ceases approximately as the square of time since first exposure (lagged 10 years).

The slope factor, indicating potency, was estimated to be 0.15 × 10−8 per year2 × fibres/mL

for the South Carolina, USA, plants and 0.018 × 10−8 per year2 × fibres/mL for the Quebec,

Canada, mines, representing exposure to chrysotile, whereas the estimate for the Patterson,

New Jersey, USA, factory where the asbestos species used was amosite was 3.9 × 10−8

per year2 × fibres/mL. In a further analysis in which fibre size was considered, the hypoth-

esis that chrysotile and amphibole forms of asbestos are equipotent was strongly rejected

(P ≤ 0.001), and the hypothesis that the potency of chrysotile asbestos was zero was not

rejected (P ≥ 0.29).

The IARC Working Group (1) noted that there is a high degree of uncertainty concerning the

accuracy of the relative potency estimates derived from the Hodgson & Darnton (60) and

Berman & Crump (64) analyses because of the severe potential for exposure misclassifica-

tion in these studies.

The study of textile workers in North Carolina, USA (7), was not included in the meta- analyses.

Based on the approach used by Hodgson & Darnton (60), the authors of the North Carolina

study (7) estimated that the percentage of deaths was 0.0098% per fibre-year/mL for workers


followed for at least 20 years. This estimate is considerably higher than the original estimate

developed by Hodgson & Darnton (60) of 0.001% per fibre-year/mL for cohorts exposed to

chrysotile.

Bourdes and coworkers (84) performed a meta-analysis of available studies on household

and neighbourhood exposure to asbestos and mesothelioma risk and came up with estimated

summary RRs of 8.1 (95% CI: 5.3–12) for household exposure and 7.0 (95% CI: 4.7–11) for

neighbourhood exposure.

IARC conclusions on mesothelioma

In respect of mesothelioma, IARC concluded that there is sufficient evidence of carcinogenic-

ity in humans for all types of asbestos, including chrysotile. This is the strongest IARC category

for describing the strength of evidence (1).

Key new studies

Hodgson & Darnton (65) updated their meta-analysis of the potency of different asbestos

fibres to cause mesothelioma following the publication of the North Carolina, USA, study (7) and revised their potency estimate upward to 0.007% per fibre-year/mL.

Of a total of 259 deaths in the Chinese asbestos factory workers (16), 2 were from mesothe-

lioma, whereas no mesotheliomas were reported among the 428 total deaths in the Chinese

chrysotile miner cohort (11). The tremolite content of the chrysotile studied in these studies

was less than 0.001%. In a brief report, it was stated that the mesothelioma incidence in the

asbestos (almost exclusively chrysotile) production areas in China was 85/1 000 000, whereas

it was 1/1 000 000 in the general population (35). It is not clear what proportion of the excess

risk observed is due to environmental exposure and what proportion is due to occupational

exposure.

Exposure to asbestos was studied among 229

malignant mesothelioma patients identified from

the Australian Mesothelioma Registry and diag-

nosed between 2010 and 2012. For 70, no

occupational exposure was discovered; these

included 37 who had performed a major reno-

vation of their housing with asbestos-containing

materials, 35 who had lived in a house during

a renovation with asbestos-containing materi-

als, 19 who had lived in a house built of fibro

(asbestos cement sheet), 19 who had lived with

someone working in an asbestos-exposed job,

12 who had performed brake/clutch work (non-

professionally), 10 who had visited Wittenoom

(the western Australian city with a crocidolite

mine) and 8 who lived in the vicinity of an asbes-

tos mine or asbestos products factory (total does

not add to 70 because a number of participants

were counted in more than one category) (85).


In a case–referent study in the United Kingdom, exposure to asbestos was studied by detailed

interview of 622 mesothelioma patients and 1420 population referents. The OR for living with

an exposed worker before the age of 30 years was 2.0 (95% CI: 1.3–3.2). No information was

available on the fibre type (86).

The prevalence of malignant pleural mesothelioma was elevated in the vicinity of a chry-

sotile asbestos plant in north Cairo, Egypt. The increased prevalence was limited to the

immediate vicinity of the factory and people estimated to have had a cumulative exposure of

20 fibre-years/mL (87). (This study was not included in the meta-analysis of Goswami and co-

workers (88) described below.)

In a cohort study of inhabitants of 15 villages in Turkey with environmental asbestos exposure

and 12 villages with no such exposure, there were 14 deaths from mesothelioma in men out

of a total of 79 cancer deaths; for women, the number of mesothelioma deaths was 17 out of

a total of 40 cancer deaths. The estimated lifetime asbestos exposure range was 0.19–4.61

fibre-years/mL; the fibre type was either tremolite or a mixture of tremolite + actinolite + chry-

sotile or anthophyllite + chrysotile (69). (This study was not included in the meta-analysis of

Goswami and co-workers (88) described below.)

In a meta-analysis of 12 cohort and case–referent studies on mesothelioma after domes-

tic exposure to asbestos, Goswami and coworkers (88) estimated a summary RR of 5.02

(95% CI: 2.48–10.13). In six studies, the fibre type was not specified; in one, it was chryso-

tile; and in four, it was chrysotile with other fibres.

AsbestosisOf 8009 deaths among Quebec, Canada, miners and millers in 1972–1992, 108 were caused

by pneumoconiosis (3). In the South Carolina, USA, cohort, the SMR for pneumoconiosis

and other pulmonary diseases was 4.81 (95% CI: 3.84–5.94), and that for asbestosis, 232.5

(95% CI: 162.8–321.9); there were 36 deaths from asbestosis and 86 from pneumoconiosis

out of a total of 1961 deaths (6). In the North Carolina, USA, chrysotile textile worker cohort,

the SMR for pneumoconiosis was 3.48 (95% CI: 2.73–4.38) (7).

The SMR for asbestosis in the Chinese chrysotile textile cohort was 100 (95% CI: 72.55–137.83)

(14). In the Balangero, Italy, mine cohort, there were 21 cases of asbestosis out of a total of

590 deaths (5).

One should note, however, that the pneumoconioses have never been reliably recorded as

a cause of death on death certificates. Additionally, mortality studies are generally not suffi-

cient to detect clinically significant morbidity. Equally, in studies of morbidity, the etiological

or diagnostic specificity of the usual methods of assessment (i.e. chest radiography, physi-

ological testing and symptom questionnaire) is limited. Many studies show that exposure to

chrysotile induces decrement in lung function, radiological changes consistent with pneumo-

coniosis and pleural changes (2).

A dose-related reduction in vital capacity (P = 0.023) and expiratory volume (P < 0.001) was

observed with increasing cumulative exposure (i.e. > 8 fibre-years/mL) to chrysotile asbestos

in miners and millers in Zimbabwe who were exposed for more than 10 years (89).

Occupational exposure to chrysotile also causes non-malignant lung diseases


Chest X-ray changes among textile and friction product workers in China were reported by

Huang (90). A cohort of 824 workers employed for at least 3 years in a chrysotile products fac-

tory from the start-up of the factory in 1958 until 1980, with follow-up through to September

1982, was studied. Overall, 277 workers were diagnosed with asbestosis during the follow-up

period, corresponding to a period prevalence of 31%. Exposure–response analysis, based on

gravimetric data converted to fibre counts, predicted a 1% prevalence of Grade I asbestosis

at a cumulative exposure of 22 fibre-years/mL.

Asbestosis was also detected in 11.3% of wives of asbestos-exposed shipyard workers with

a 20-year work history and in 7.6% of their sons. The asbestos type was not specified (91). One or more radiological signs of asbestosis were observed in 35% of the household con-

tacts of amosite asbestos insulation workers (92). The prevalence of pleural calcifications was

increased 10.2-fold (95% CI: 2.8–26.3) among blood relatives of workers in chrysotile asbes-

tos factories and 17.0-fold (95% CI: 7.7–32.2) among people living in the vicinity of a factory

using Russian and Canadian chrysotile asbestos (93).

IPCS conclusions

In addition to lung cancer and mesothelioma, occupational exposure to chrysotile also causes

non-malignant lung diseases that result in deterioration in lung function, in particular a form

of lung fibrosis described by the term asbestosis (2).


Global burden of diseaseNo studies are available specifically on the global burden of disease caused by chrysotile.

However, more than 90% of all asbestos used historically and practically all asbestos used

today is chrysotile; thus, the estimates made of the populations exposed to asbestos are

largely directly valid for chrysotile.

Cancer of the lung

Based on the methods of Driscoll et al. (33), the burden of disease estimate for lung can-

cer was updated by Prüss-Üstün and collaborators (94). Using the combined relative risk

(SMR 2.0) of lung cancer in 20 cohort studies published by 1994 (95) and the estimated

proportion of the population actually exposed to asbestos in the different WHO regions, Prüss-

Üstün and collaborators (94) estimated that in the year 2004, asbestos caused 41 000 lung

cancer deaths and 370 000 disability-adjusted life years (DALYs).

In an effort to estimate the global lung cancer burden from exposure to asbestos, McCormack

and co-workers (96) studied the ratio of excess lung cancer deaths to excess mesothelioma

deaths associated with exposure to different asbestos fibre types. This ratio was 6.1 (95% CI:

3.6–10.5) in the 16 available chrysotile-exposed cohorts. The authors were not able to derive

an estimate for the total number of deaths or DALYs for asbestos-induced lung cancer. They

concluded that in exposure to chrysotile, the observation of few mesothelioma deaths cannot

be used to infer “no excess risk” of lung or other cancers.

Mesothelioma

Driscoll and co-workers (33) estimated the global burden of mesothelioma deaths and DALYs

based on the notion that mesothelioma is nearly always caused by exposure to asbestos, using

the proportion of workers in different economic sectors (agriculture, mining, manufacturing,

electrical, construction, trade, transport, finance and services) who are exposed to asbestos

in Europe, the population numbers in these subsectors, as developed in the CAREX database

by the Finnish Institute of Occupational Health, and an average mesothelioma risk for differ-

ent asbestos species from the study of Hodgson & Darnton (60). The global burden estimates,

updated for the year 2004 worldwide, were 59 000

deaths and 773 000 DALYs from malignant meso-

thelioma (33, 97).

Asbestosis

Driscoll and co-workers (98) estimated the global

burden of asbestosis deaths and DALYs based on

the notion that asbestos is the only cause of asbes-

tosis, using the proportion of workers in different

economic sectors (agriculture, mining, manufactur-

ing, electrical, construction, trade, transport, finance

and services) who are exposed to asbestos in

Europe, the population numbers in these sub-

sectors, as developed in the CAREX database by

the Finnish Institute of Occupational Health, and

In the year 2004, asbestos caused 41 000 lung cancer deaths


published risks of developing asbestosis at different levels of exposure to chrysotile (99). The

global burden estimates for the year 2000 worldwide were 7000 deaths and 380 000 DALYs

from asbestosis.

Chrysotile substitute fibres5

A WHO Workshop on Mechanisms of Fibre Carcinogenesis and Assessment of Chrysotile

Asbestos Substitutes (100) was convened at IARC in Lyon, France, in response to a request

from the Intergovernmental Negotiating Committee for the Rotterdam Convention on the Prior

Informed Consent Procedure for Certain Hazardous Chemicals and Pesticides in International

Trade (INC). The substitutes considered by the WHO workshop included the 12 chrysotile

substitutes identified by the INC for priority assessment by WHO, 2 substances from a second

list provided by the INC to be assessed if resources allow and 1 further substance for which

data were submitted in response to WHO’s public “call for data” for the workshop.

Methodological aspects

The workshop established a framework for hazard assessment based on epidemiological data,

in vivo experimental animal data on carcinogenicity and potential to cause lung fibrosis, and

mechanistic information, genotoxicity data and biopersistence data as determinants of dose

at the target site and possible indicators of carcinogenic potential. Noting that substitutes may

be used in a variety of applications with different exposure potential, either alone or in com-

bination with other substances, the workshop did not embark on risk assessment, but rather

limited its work to assessing the hazard.

The workshop concluded that epidemiological studies on fibres have a clear advantage over

toxicological studies, in that they involve studies of humans. They also have the advantage that

they study the effects of exposure in the real world, where the effects of these exposures may

5 This section is largely taken from reference 100.


be mitigated or enhanced by other factors. Despite these obvious advantages, the presence

or absence of evidence of risk from epidemiological studies does not always override contrary

findings from toxicological studies. The interpretation of either positive or non-positive epide-

miological findings needs to be carefully considered in light of the strengths and weaknesses

of the study design.

Carcinogenic response in experimental animals (lung cancer, mesothelioma) and fibrosis

were considered to be the key effects; epithelial cell proliferation and inflammation were

not regarded to be equally important indicators of human health hazard. From studies with

asbestos, it is apparent that the sensitivity of the rat to fibre-induced lung tumours in inhala-

tion studies is clearly lower than that of humans. This holds true when the effect is related to

exposure concentrations and lung burdens. In comparison, testing of fibres by intraperitoneal

injection represents a useful and sensitive assay, which also avoids the confounding effects

of granular dusts.

Fibres may act in principle on all steps in tumour development. However, of these interac-

tions, the in vitro genotoxicity tests are mainly indicative of genotoxic effects involved in the

first steps of tumour initiation. Effects related to biopersistence of fibres (e.g. continuous

“frustrated phagocytosis”) and secondary genotoxicity arising from reactive oxygen and nitro-

gen species and mitogen release by macrophages and inflammatory cells are not detected in

routinely used genotoxicity tests. Therefore, negative results indicate a lack of primary geno-

toxicity, but do not exclude effects on later steps of carcinogenesis.

The chemical composition of the substitutes is a key factor influencing their structure and

physicochemical properties, such as surface area, surface reactivity and solubility. Attention

should be paid not only to the chemical composition of the fibres, including their major

and trace elements, but also to contaminants or accompanying elements, including their

speciation. Fibre-derived free radical

generation favours DNA damage and

mutations. Surface properties are a

determining factor in the inflammatory

response. In relation to fibre dimen-

sion and deposition, one can assume

that there exists a continuous variation

in the carcinogenic potency of respira-

ble fibres, which increases with length.

Biopersistence of a fibre increases tissue

burden and therefore may increase any

toxicity the fibre might possess. For syn-

thetic vitreous fibres, there is evidence

in experimental animals that the poten-

tial for carcinogenicity increases with

biopersistence. This has not been dem-

onstrated, however, for other fibres. For

all fibres, the fibres must be respirable to

pose an appreciable hazard.

Respirability is mainly determined by

diameter and density; thus, with a given

The global burden estimates for the year 2000 worldwide were 7000 deaths and 380 000 DALYs from asbestosis


fibre diameter, a higher specific density is associated with lower respirability (note that the

specific density of most organic fibres is lower than the specific density of inorganic fibres).

Hazard assessment

The workshop decided to group substitutes roughly into hazard groupings of high, medium

and low. However, for some substitutes, there was insufficient information to draw any con-

clusion on hazard; in these cases, the workshop categorized the hazard as indeterminate (a

category that is not comparable to the other groupings). The hazard groups high, medium and

low should be considered in relation to each other and do not have reference to formal crite-

ria or definitions, as such. It is important to note that for each substitute, the fibre dimensions

of commercially available products may vary, and the workshop did not assess this variation.

The substitutes are listed below in alphabetical order.

para-Aramid releases respirable fibres with dimensions similar to those of known carcino-

genic fibres. p-Aramid fibres have induced pulmonary effects in animal inhalation studies.

Biopersistence was noted. The workshop considered the human health hazard to be medium.

Most natural deposits contain attapulgite fibres that are less than 5 μm in length; at work-

places, the mean fibre length was less than 0.4 μm. The hazard from exposure to respirable

attapulgite is likely to be high for long fibres and low for short fibres. This assessment is mainly

based on findings in long-term inhalation experiments in animals, in which tumours were seen

with long fibres; no tumours were seen in studies with short fibres.

The nominal diameter of carbon fibres ranges from 5 to 15 μm. Workplace exposure in pro-

duction and processing is mostly to non-respirable fibres. The workshop considered the

hazard from inhalation exposure to these fibres to be low.


Most cellulose fibres are not respirable; for these, the hazard is low. For respirable fibres,

the available data do not allow the evaluation of the hazard; the hazard is thus indeterminate.

The dimensions of graphite whiskers indicate high respirability, and they have a long half-time

in the lungs. However, in the absence of any further useful information, the hazard from inha-

lation exposure was considered to be indeterminate.

Magnesium sulfate whiskers did not induce tumours in limited inhalation and intratracheal

administration studies, were negative in limited short-term tests and are very quickly eliminated

from the lung. It was discussed whether the hazard grouping should be low or indeterminate.

On the basis of the data available, in the time available, consensus was not reached.

For respirable polyethylene, polyvinyl chloride and polyvinyl alcohol fibres, the data were

insufficient for hazard classification, and the working group thus considered the hazard

indeterminate.

In facilities producing polypropylene fibres, exposure to respirable fibres occurs. After intratra-

cheal administration, respirable polypropylene fibres were highly biopersistent; however, no

fibrosis was reported in a subchronic animal study. However, the data are sparse, and the

human health hazard potential was considered to be indeterminate.

The workshop considered that respirable potassium octatitanate fibres are likely to pose a high hazard to humans after inhalation exposure. At workplaces, there is exposure to respirable

fibres. There was a high and partly dose-dependent incidence of mesothelioma after intraperi-

toneal injection in two species (high incidence indicating high potency). There is evidence of

genotoxicity. Biopersistence was noted.

The fibres must be respirable to pose an appreciable hazard


Wool-like synthetic vitreous fibres (including glass wool/fibrous glass, mineral wool, special-

purpose vitreous silicates and refractory ceramic fibre) contain respirable fibres. For these

fibres, the major determinants of hazard are biopersistence, fibre dimensions and physico-

chemical properties. It was noted that the available epidemiological data are not informative,

due to mixed (vitreous fibre) exposures or other design limitations. Based on inhalation expo-

sure studies, intraperitoneal injection studies and biopersistence studies, it was concluded

that the carcinogenic hazard could vary from high to low, with high for the biopersistent fibres

and low for the non-biopersistent fibres.

Natural wollastonite contains respirable fibres. In occupational settings, exposure is mainly

to short fibres. In chronic studies, wollastonite did not induce tumours after intraperitoneal

injection in animals; however, samples of wollastonite were active in different studies for ge-

notoxicity. After considering this apparent discrepancy, it was concluded that the hazard was

likely to be low.

In a limited study with intraperitoneal implantation, xonotlite did not induce tumours. After

intratracheal injection in a chronic study, no inflammatory or fibrotic reaction of the lung was

observed. The chemical composition of xonotlite is similar to that of wollastonite, but it is

more rapidly eliminated from the lung. The workshop considered the human health hazard

to be low.


Tabl

e 1.

Key

find

ings

of t

he c

ohor

t stu

dies

on

the

adve

rse

heal

th e

ffect

s of

chr

ysot

ile a

sbes

tos

Indu

stry

and

loca

tion

Expo

sure

to c

hrys

otile

Ex

posu

re to

oth

er fi

bres

Deat

hs fr

om

all c

ause

sLu

ng c

ance

r de

aths

SM

R (9

5% C

I)

Mes

othe

liom

a de

aths

SM

R (9

5% C

I)

Pneu

moc

onio

sis/

as

best

osis

de

aths

Refe

renc

es

Chr

ysot

ile m

inin

g/m

illin

g in

Que

bec,

Can

ada

Ave

rage

60

0 fi

bre-

year

s/m

L< 1

% t

rem

olit

e8

00

96

57

1

.37

(1

.27

–1.4

8)

38

10

8/N

D3,

60

Fric

tion

pro

duct

s fa

ctor

y in

Con

nect

icut

, U

SA

Ave

rage

46

fibr

e-ye

ars/

mL

Som

e an

thop

hylli

te in

use

du

ring

the

last

20

yea

rs o

f fo

llow

-up

80

37

3

1.4

9 (

1.1

7–1

.87

)0

12

/052

, 60

Asb

esto

s te

xtile

mill

in

Ita

ly,

wom

en w

ith

com

pens

ated

asb

esto

sis

ND

“Mai

nly

chry

soti

le”a

12

39

6

.82

(3

.12

–12

.95

)N

DN

D/2

153

Asb

esto

s te

xtile

mill

s in

S

outh

Car

olin

a, U

SA

99

% <

20

0 fi

bre-

year

s/m

L,

aver

age

26

–28

fibr

e-ye

ars/

mL

0.0

4%

am

phib

oles

1 9

61

19

8

1.9

5 (

1.6

8–2

.24

)3

85

/36

6, 5

5

Asb

esto

s te

xtile

mill

s in

N

orth

Car

olin

a, U

SA

Ave

rage

(ra

nge)

17

.1

(< 0

.1–2

943.4

) fib

re-y

ears

/mL

0.0

4%

am

phib

oles

2 5

83

27

7

1.9

6 (

1.7

3–2

.20

)4

b7

3/3

67,

55,

60

Chr

ysot

ile m

ine

in

Bal

ange

ro,

Ital

y< 1

00

– ≥

40

0 fi

bre-

year

s/m

LN

o am

phib

oles

, 0

.2–0

.5%

ba

lang

eroi

te5

90

45

1

.27

(0

.93

–1.7

0)

44.

67 (1

.27–

11.9

6)N

D/2

15

Chr

ysot

ile m

ine

in

Qui

ngha

i, C

hina

Ave

rage

in 2

00

6, 2

.9–6

3.8

fib

res/

mL

≤ 0

.00

1%

am

phib

oles

42

85

6

4.7

1 (

3.5

7–6

.21

)0

cN

D11

Eig

ht c

hrys

otile

tex

tile

fa

ctor

ies

in C

hina

ND

ND

d4

96

65

5

.3 (

2.5

–7.1

)2

ND

/29

e8

Asb

esto

s m

anuf

actu

ring

fa

ctor

y in

Chi

naM

edia

n 1

, 8

and

23

fibr

es/m

L in

dif

fere

nt d

epar

tmen

ts≤

0.0

01

% a

mph

ibol

es2

59

53

4

.08

(3

.12

–5.3

3)

2N

D/3

915

ND

: no

dat

aa

No

furt

her

data

on

othe

r po

ssib

le a

sbes

tos

fibre

typ

es.

b M

esot

helio

ma

data

ava

ilabl

e on

ly f

or 1

99

9–2

00

3 o

f th

e to

tal f

ollo

w-u

p pe

riod

of

19

53

–20

03

.c

The

auth

ors

note

tha

t m

esot

helio

ma

may

be

unde

rrep

orte

d.d

The

publ

ishe

d pa

per

has

no in

form

atio

n on

the

asb

esto

s sp

ecie

s, b

ut m

ost

likel

y it

is t

he C

hine

se c

hrys

otile

wit

h < 0

.00

1%

am

phib

oles

.e

The

text

of

the

pape

r st

ates

tha

t th

ere

wer

e 1

48

cas

es o

f as

best

osis

, no

t 2

9 a

s in

the

tab

les.


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ISBN 978-92-4-256481-5

L’amiante – un groupe de minéraux comportant le chrysotile, la

crocidolite, l’amosite, l’anthophyllite, la trémolite et l’actinolite – est

l’un des produits cancérogènes les plus importants sur les lieux de

travail. Au moins 107 000 personnes meurent chaque année de

maladies liées à l’amiante, dont le cancer du poumon. Même

si son utilisation a beaucoup baissé dans de nombreux pays, le

chrysotile reste largement employé, en particulier dans les pays

en développement.

La présente publication sur l’amiante chrysotile comporte trois par-

ties. La première reproduit un bref document d’information de

l’OMS à l’intention des décideurs sur l’élimination des maladies liées

à l’amiante. La deuxième répond aux questions soulevées

couramment au cours des discussions politiques, en particulier pour

aider les décideurs. La troisième est un résumé technique des effets

du chrysotile sur la santé, réunissant et récapitulant pour la première

fois les évaluations les plus récentes de l’OMS qui font autorité et

ont été réalisées par son Centre international de recherche sur le

cancer et son Programme international sur la sécurité chimique.

Ce résumé technique passe également en revue les résultats des

principales études publiées après ces évaluations, ainsi que les

conclusions tirées des évaluations des produits de remplacement

faites par l’OMS.

Cette publication intéressera tous les responsables gouvernementaux

devant prendre des décisions éclairées sur la gestion des risques sani-

taires liés à l’exposition à l’amiante chrysotile.

Département Santé publique, environnement et déterminants sociaux de la santé (PHE)

Santé de la famille, de la femme et de l’enfant (FWC)

Organisation mondiale de la Santé (OMS)

Avenue Appia 20 – CH-1211 Genève 27 – Suisse

www.who.int/phe/fr/

www.who.int/ipcs/fr/

Courriel : [email protected]

SANTÉ PUBLIQUE ET ENVIRONNEMENT